Macromolecule Transport - an overview (2023)

macromolecule transport), small pores (5 nm; micromolecule transport), and ultra-small pores (water transport).

From: Critical Care Nephrology (Second Edition), 2009

Related terms:

  • Lymphedema
  • Caveolae
  • Elastin
  • Peyer's Patch
  • Lymph Duct
  • Patient
  • Weight Loss
  • ABC Transporter
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Pathophysiology and Molecular Research in Lymphedema

Babak J. Mehrara, ... Raghu P. Kataru, in Principles and Practice of Lymphedema Surgery (Second Edition), 2022

Pathophysiology of Primary Lymphedema

DNA sequencing studies have identified genetic abnormalities in patients with primary lymphedema.1–8 These genetic defects can be transmitted in families as a result of germline mutations or can develop from spontaneous somatic mutations.9 Genetic defects in patients with primary lymphedema have a broad range of effects: abnormal expression or function of growth factors that regulate lymphatic growth and repair, lymphatic valve abnormalities, leaky lymphatics, and changes in lymphatic smooth muscle cells. It is important to note, however, that the genetic defects that cause the development of lymphedema in most patients with primary lymphedema remain unknown. Nevertheless, the most common cause of primary lymphedema is deficits in the number and function of collecting lymphatics. These defects likely are present at birth and worsen over time, eventually resulting in overt lymphedema development.

The timing and severity of primary lymphedema are highly variable and may be modulated by the penetrance of genetic abnormalities, environmental factors, or hormonal fluctuations. For example, patients with subtle genetic lymphatic abnormalities may be asymptomatic due to the excess capacity of the lymphatic system to transport macromolecules. However, additional insults to the lymphatic system—for example, surgical injury or obesity—may lead to further declines in lymphatic function and overt development of lymphedema. In other patients with germline mutations of the lymphatic system, genetic abnormalities may have limited penetrance and involve only a subset of lymphatic channels. These patients may develop lymphedema later in life, as the pathophysiology of the disease advances to a point where the capacity of the lymphatic system to transport macromolecules is exceeded. Thus, the timing of lymphedema development in primary lymphedema is variable, with some patients exhibiting the disease shortly after birth—congenital lymphedema—or, more commonly, disease development later in life, termed lymphedema praecox or lymphedema tarda.

Congenital lymphedema, most commonly manifesting as lower extremity swelling in female patients, accounts for approximately 10–25% of all cases of primary lymphedema.3 These patients have variable severity of the disease, with some exhibiting mild swelling, while others display severe pathology. Further, primary lymphedema may present unilaterally or bilaterally, with differential severity between limbs. Milroy disease is a familial, sex-linked disease and is the classic form of congenital lymphedema, accounting for 2–3% of all patients with congenital primary lymphedema.10 Patients with Milroy disease have heterozygous inactivating mutations of vascular endothelial growth factor receptor 3 (VEGFR3) and usually present with leg swelling and chylothorax shortly after birth. VEGFR3 activation by its ligands—vascular endothelial growth factor C (VEGF-C) and VEGF-D—is a critical mechanism regulating lymphatic endothelial cell differentiation, proliferation, migration, and function. Homozygous mutations of VEGFR3 are embryologically lethal in mice; in contrast, heterozygous inactivating mutations allow for some lymphatic development. As a result, patients with Milroy disease have hypoplastic lymphatic vessels of the extremities, usually affecting the lower extremities more severely.

Lymphedema development before the age of 35 is referred to as lymphedema praecox. Patients with this form of lymphedema are most commonly female (ratio of females to males is 4:1) and usually develop unilateral lower extremity lymphedema around the time of puberty. The timing of disease development and its overlap with female hormone fluctuations have led some investigators to hypothesize that sex hormones may play a role in disease development/progression.3 However, the cellular mechanisms that regulate this response remain unknown, and only a few studies have investigated the role of female sex hormones in regulating lymphatic function. Pathologically, most patients with lymphedema praecox have fewer initial lymphatics and hypoplastic collecting vessels—although the severity of the disease is highly variable.

Patients who develop primary lymphedema after the age of 35 have lymphedema tarda. This presentation of primary lymphedema is infrequent and is a diagnosis of exclusion. Lymphedema tarda most commonly involves the lower extremity of women, and the genetic causes of the disease remain largely unknown. However, recent genetic studies have shown that some patients with lymphedema tarda have mutations in FOXC2, a gene that regulates lymphatic valve development.11–13

Most researchers concede that an arbitrary classification of primary lymphedema based on the age at which symptoms present is not particularly helpful when evaluating individual patients. This approach does not, for example, delineate the primary pathophysiology of the disease and is therefore not useful for developing targeted interventions. Instead, most patients are treated with palliative measures such as compression and physiotherapy, aiming to prevent disease progression. More recent studies have developed classification schemes that combine the clinical presentation of the disease with genetic sequencing.14 This approach categorizes congenital lymphedemas into five main groups: syndromic, systemic or visceral, disturbed growth, congenital onset, and late onset. This classification is more precise and provides more pathological information that may aid diagnostic or therapeutic interventions.

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(Video) Macromolecule transport

The Peritoneal Dialysis System

Claudio Ronco, in Critical Care Nephrology (Second Edition), 2009

The Peritoneal Dialysis Membrane

The peritoneal dialysis membrane is a living structure that can be considered more a functional barrier than a precisely defined anatomical structure. On the basis of the flow/clearance curve described previously, the following question may arise: Why is the value of the mass transfer coefficient (MTC) so low in peritoneal dialysis compared with other dialysis treatments, and is the membrane involved in such limitations?

The three-pore model of peritoneal transport has been proposed by Rippe and associates13 to explain the peculiar behavior of the peritoneal membrane in relation to macromolecules, micromolecules, and water transport. According to this model, human peritoneum appears to behave as a membrane with a series of differently sized pores as follows: large pores (25 nm; macromolecule transport), small pores (5 nm; micromolecule transport), and ultra-small pores (water transport). The anatomical structure of these ultra-small pores corresponds to the “water channels” created by a specific protein “aquaporin” acting as a carrier for water molecules. This model locates the main resistance to transport at the level of the capillary wall, regarding all other anatomical structures as a negligible site of resistance. Later the interstitium was added as an additional site of resistance.

A controversial opinion is offered by the so-called “distributed model” offered by Dedrick and colleagues.14 In this model, the main resistance to transport is apparently located in the interstitial tissue. This anatomical entity consists of a double-density material containing water and glycosaminoglycans in different proportions. The interstitial matrix seems to act as the main site of resistance to solute and water transport from the bloodstream to the peritoneal cavity. The solute diffusivity in free water is greater than that in the tissue by more than one order of magnitude. Accordingly, not only the structure of the interstitium but also the thickness of the glycosaminoglycan layer may play an important role in restricting the diffusive transport of solutes. There is a certain discrepancy between the two models, and overall transport process is probably governed by a more complex and integrated series of events, each with a remarkable but not absolute importance. The pressures applied to the system that contribute to the generation of the transmembrane pressure are shown in detail in Figure 264-3. It is evident that the osmotic pressure generated by the glucose contained in the dialysate is by far the most important. Nevertheless, as shown in Figure 264-4, because the peritoneal membrane is not a perfect barrier for the employed osmotic agent (glucose), the transmembrane pressure gradient is continuously varying in relation to the velocity of reabsorption of glucose from dialysate into the blood compartment. Furthermore, capillaries, which are located at different distance from the mesothelial barrier, may be exposed to different concentrations of readsorbed glucose with different levels of cell damage (Fig. 264-5).

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Lymphedema

Babak J. Mehrara, ... Raghu Kataru, in Plastic Surgery - Principles and Practice, 2022

(Video) Biomolecules (Updated)

Risk Factors for Lymphedema

There are many known risk factors for the development of lymphedema, including obesity, radiation, infection, advanced age, and genetic factors. Obesity has long been recognized as an important risk factor for the development of lymphedema following cancer surgery. For example, Helyer etal found that patients with a body mass index (BMI) of greater than 30 had a more than threefold increase in the risk of developing lymphedema following breast cancer treatment as compared with patients with a BMI less than 25.2 McLaughlin etal examined breast cancer patients treated with either sentinel lymph node biopsy or axillary lymph node dissection and found those with a higher baseline BMI had a significantly higher incidence of lymphedema.1 Interestingly, these authors found that even postoperative weight gain (independent of the presurgical weight) significantly increased the risk of lymphedema development. Importantly, a randomized, controlled, prospective trial showed that patients who had nutritional counseling and lost weight over a 12-week period of time had significant reductions in their upper extremity limb volumes as compared to a control group that did not receive nutritional counseling and did not lose weight.3 Other studies have shown that exercise programs improve lymphedema symptoms at least in part by promoting weight loss. These findings are supported by prospective longitudinal studies demonstrating that the incidence of lymphedema is increased nearly twofold in patients with a sedentary lifestyle.

Several lines of evidence support the idea that obesity may increase the risk of lymphedema by decreasing lymphatic function. For example, macromolecule transport in obese patients is significantly decreased as compared with healthy volunteers.4 Other studies have shown that obese patients (BMI >59) spontaneously develop lower extremity lymphedema even without surgery or other injuries.5 Preclinical studies have shown that increasing obesity is linearly correlated with impaired lymphatic pumping capacity, lymphatic vessel number, and lymphatic vessel leakiness.6 These changes are partially reversible with exercise or weight loss. Taken together, these findings suggest that weight loss and exercise programs may be beneficial in patients who are considered for lymphatic surgery since these behavioral modifications improve lymphatic function and regeneration.

Radiation therapy, mainly when used as adjuvant therapy in conjunction with surgical extirpation, is also a significant risk factor for the development of lymphedema increasing the relative risk of disease two- to fivefold. Radiation in isolation rarely (<7%) results in lymphedema development.7 However, radiation and obesity appear to increase the risk of lymphedema in an additive manner since the risk of disease development is significantly higher in obese patients treated with adjuvant radiotherapy. Some researchers have questioned the link between radiation and development of breast cancer-related lymphedema, having failed to show a significant increase in risk in some studies. However, it is likely that these studies are confounded by the fields used for radiation and heterogeneous populations of patients that had radiation treatment to the chest wall rather than regional lymph node basins.

Postoperative infections and cellulitis have also been linked to the development of lymphedema following lymph node dissection for a variety of cancers. This clinical finding is supported by recent studies demonstrating that bacterial toxins and inflammatory responses can permanently injure lymphatic endothelial cells and lymphatic smooth muscle cells. Other studies have shown that lymphatic injury can result in impaired innate and adaptive immune responses, thereby increasing the risk of infections.8 Thus, patients with lymphatic injury are at high risk for developing infections and when these infections develop, they may cause additional injury to the lymphatic system, thereby setting up a vicious cycle that leads to rapid progression of the disease.

Advanced age also infers increased risk of developing lymphedema in some series. One study of 287 Australian breast cancer survivors showed that women who were more than 50 years old were 3.1 times more likely to develop lymphedema following axillary lymph node dissection as compared with those who were less than 50 years old at the time of surgery.9 However, the importance of age as a predictive factor for lymphedema development is debated, as other studies have failed to show a significant correlation. Nevertheless, recent preclinical studies have shown that aging decreases lymphatic pumping capacity, lymphatic permeability, and lymphatic endothelial cell proliferation potential with resultant decreased lymphatic function. It is therefore conceivable that these physiological changes may infer a higher risk of developing lymphedema after surgery.

Recent studies have identified genetic mutations and alternative coding regions that increase the risk of secondary lymphedema development. For example, Finegold etal showed that mutations in the connexin 47 or hepatocyte growth factor genes significantly increased the risk of breast cancer-related lymphedema.10 Other studies have shown that normal variants of four genes, so-called single-nucleotide polymorphisms (SNPs), confer a significant risk for the development of secondary lymphedema following axillary lymph node dissection for breast cancer treatment. A recent meta-analysis reviewed reports of the association of secondary lymphedema and genetic variations in coding sequences of 18 genes, including HGF, MET, GJC2, IL1A, IL4, IL6, IL10, IL13, VEGF-C, NFKB2, LCP-2, NRP-2, SYK, VCAM1, FOXC2, VEGFR2, VEGFR3, and RORC.11 Taken together, these studies demonstrate that lymphedema is a complex disease and that the risk of this disease can be modified by intrinsic and extrinsic risk factors. It is also clear that these independent variables interact with each other, further modulating the risk of disease development.

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Exploring the choroidal vascular labyrinth and its molecular and structural roles in health and disease

J. Brinks, ... C.J.F. Boon, in Progress in Retinal and Eye Research, 2022

2.6.4 Transendothelial channels, vesiculo-vacuolar organelles, and coated pits

Electron microscopy studies using mouse tissues suggest that the fusion of caveolae forms transendothelial channels and vesiculo-vacuolar organelles (i.e. networks of interconnecting vesicles), which serve a function similar to caveolae to transport macromolecules (Gu et al., 2017; Klaassen et al., 2013; Nakanishi et al., 2016; Tse and Stan, 2010). However, their relationship to caveolae has been disputed, as these structures can still form in mice lacking Cav1, the principal component in caveolae (Nakanishi et al., 2016; Tse and Stan, 2010). Transendothelial channels are 60–80-nm openings that span the cytoplasm from the apical side of the cell to the basal side of the cell, and can be covered at both sides by PLVAP (Bosma et al., 2018; Nakanishi et al., 2016; Tse and Stan, 2010). Interestingly, these channels have been shown to facilitate the extravasation of leukocytes from the circulation into tissues during inflammation (Bosma et al., 2018; Keuschnigg et al., 2009). PLVAP, which is heavily expressed on cell membranes at the site of transmigration, appears to play an essential role in this process, as blocking PLVAP using a monoclonal antibody in a mouse model of acute inflammation reduced the transmigration of leukocytes by 85% (Keuschnigg et al., 2009). Transendothelial channels can also transport relatively large plasma proteins such as albumin across CECs, suggesting that either they do not contain diaphragm filters formed by PLVAP or that the filter can open and close (Nakanishi et al., 2016; Tse and Stan, 2010). Like transendothelial channels, evidence suggests that the permeability of vesiculo-vacuolar organelles, which appear as multiple fused vesicles on electron microscopy, can also be modulated. Interestingly, experiments with mice suggested that VEGF and histamine ‒ which is produced in the human choroid by mast cells ‒ may serve to increase vascular permeability by acting on vesiculo-vacuolar organelles (Dvorak and Feng, 2001). Coated pits, which are present in the choriocapillaris, are specialised patches of receptor proteins at the cell surface that invaginate upon ligand binding and mediate transendothelial transport via endocytosis (Nakanishi et al., 2016). Although coated pits have been suggested to play a role in transporting low-density lipoproteins, their exact function is currently unknown, as both caveolae and transendothelial channels have been shown to transport these lipoproteins as well (Nakanishi et al., 2016).

In summary, transendothelial channels, vesiculo-vacuolar organelles, and coated pits are all present in CECs and serve to transport macromolecules and leukocytes (Bosma et al., 2018; Klaassen et al., 2013; Nakanishi et al., 2016). Future research regarding the specific functions of each of these specialised structures is needed in order to understand how they relate to and/or interact with caveolae and PLVAP, thus yielding new insights into how CECs transport nutrients and the role of these structures in specific chorioretinal diseases.

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(Video) Transport Proteins: Pumps, Channels, Carriers

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Scientific Foundations of Clinical Practice, Part II

F. Sessions Cole MD, ... Aaron Hamvas MD, in Pediatric Clinics of North America, 2006

Loss-of-function mutations in ABCA3 disrupt pulmonary surfactant metabolism by altering composition of surfactant phospholipid in both newborn infants and older children [7,8,19,59,105]. ABCA3 is a 180- to 200-kd protein that is a member of a superfamily of proteins that transport macromolecules across membranes [7,106]. ABCA3 encodes an ATP-binding cassette transporter that has been localized to the limiting membrane of lamellar bodies of type 2 pneumocytes [7,19]. It is likely that ABCA3 is involved in transport of phospholipids into the lamellar body in type 2 pneumocytes that may be required for assembly of the pulmonary surfactant [58]. Recent studies of lung tissue from 10 of 14 infants who had unexplained respiratory distress syndrome also suggest a role for ABCA3 in processing of surfactant proteins B and C [105]. Twelve distinct loss-of-function mutations in this gene have been reported recently in 16 of 21 patients who had severe, otherwise uncharacterized neonatal respiratory distress who were part of a larger cohort (n = 337 infants) with severe respiratory distress accumulated by national and international referral [19]. Dense lamellar body appearance, abnormalities in surfactant phospholipid composition, and severe surfactant dysfunction have been reported in an additional 8 infants with these mutations [59]. Older infants and children have been reported recently with ABCA3 mutations, an observation that suggests greater genotype–phenotype diversity than observed in affected newborn infants [7,8,60]. The disruption of lamellar body organization is associated with disruption of processing rather than deficiencies of surfactant proteins B and C in a limited number of infants evaluated to date [59,105]. These data suggest that mutations in ABCA3 disrupt the pulmonary surfactant metabolic pathway through effects on phospholipid transport.

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Pathogenesis of Alcohol-Associated Liver Disease

Natalia A. Osna, ... Kusum K. Kharbanda, in Journal of Clinical and Experimental Hepatology, 2022

(Video) Vesicular Transport | Endocytosis and Exocytosis

Extracellular vesicles (EVs) as diagnostic tools

EVs are small membrane-bound vesiclesthat contain proteins, lipids, and/or nucleic acids as part of their cargo. These vesicles are subdivided into three groups: exosomes, micro-vesicles, and apoptotic bodies. Inside cells, intraluminal vesicles are formed by components of the endosomal-sorting-complex-required-for-transport machinery, lipids, and tetraspanins (e.g., CD63, CD81, etc.).276 When multivesicular bodies dock and fuse with the plasma membranethese intraluminal vesicles are also released as exosomes.276 The usual sizes of exosomes is 30–150nm, while apoptotic bodies with the size of 1–5μM are the largest. EVs establish the connection between the donor (EV-producing) and recipient (EV-capturing) cells. EVs’ half-life in the circulation is quite short (up to 6h) since they are readily captured by target cells and are important intercellular messengers involved in organ-to-organ communications.277

Alcohol consumption substantially increases EV biogenesis and secretion from liver cells and also affects their contents.278,279 The number of circulating EVs in plasma samples of acute alcoholic hepatitis patients was found to be highercompared with EV levels in healthy donors.280 EV content comprises DNA, protein, lipids cargo, metabolites, mRNA, and noncoding RNA. Since EV cargo is organ- and disease-specific, circulating EVs can be used as “barcodes” that display not only their tissue of origin but also allow differential diagnosis of alcohol misuse and disease state.281 Biomarkers, including cytokeratin-18, vanin-1, asialoglycoprotein receptor- 1 and specific microRNAs (miRNAs) indicate a liver-specific origin.282–284

Various studies have shown the importance of EV cargo-mediated ethanol-initiated crosstalk between hepatocytes and macrophages in inflammation development via their ability to transport macromolecules, including regulatory miRNAs, between cells of different organs.

To this end, hepatocyte-derived EVs express CD40L that activates macrophages in a caspase 3-dependent manner and induces a proinflammatory macrophage phenotype.285 Furthermore, EVs released from alcohol-exposed macrophages induce MCP-1 expression in naive hepatocytes to promote infiltration of circulating macrophages into the liver.286 Additional studies comparing the EVs generated by hepatocytes isolated from livers of mice fed control or ethanol diets, demonstrated that heat shock protein 90 (HSP 90) is expressed and transported with exosomes, which causes increased expression of the proinflammatory cytokines, TNFα and IL-1β, and suppression of anti-inflammatory markers, CD163 and CD206, on macrophages.287 The same authors demonstrated that these effects were reversed by HSP 90 inhibitor treatment.287

In addition, the transfer of nucleic acid cargo in EVs also plays a pathophysiological role in liver inflammation.278 The increase in the levels of miR122, miR192, and miR30a in EVs were observed in mice chronically fed ethanol diet and alcoholic hepatitis patientswith the highest diagnostic accuracy for miR192.288 Further studies documented that hepatocytes exposed to alcohol secrete exosomes containing miR122 which sensitizes liver macrophages to the effects of LPS.288 Furthermore, the increased miR122, miR155 and miR-146a levels in exosomes correlated with elevated ALT levels in various mouse models of liver injury induced by alcohol, acetaminophen or TLR9 ligands.289

Importantly, EV levels and cargo allow differentiation of various stages of ALD, from fatty liver to mild alcoholic steatohepatitis.290,291 Isolated hepatocytes and macrophages from mice at an early stage of disease release more EVs, with distinct miRNA profiles, such as let-7f, miR29a, and miR340290,291. The progression of ALD from mild alcoholic hepatitis to severe injury with features of ballooning cell degeneration and liver fibrosis was associated with the release of EVs carrying profibrotic miR221, miR126, and miR27, which are unique for this disease stage and can be used as a barcode.291 An increase of mitochondrial (mt) DNA in EVs was observed at this late stage of ALD, which by binding to TLR9 promotes proinflammatory activation.291 As documented, TLR9 antagonist repressed the production of IL-17, but not IL-1β induced by EVs, which contributes to inflammation and liver injury.291 The importance of EV-contained mtDNA and TLR9 signaling for ALD progression was also demonstrated in acute-on-chronic mouse ALD model, where mtDNA-enriched microparticles released from hepatocytes promoted neutrophilic inflammation via activation of TLR9, leading to hepatic damage.292

High levels of the EtOH-metabolizing enzyme, CYP2E1, in exosomes have also been characterized as barcodes for alcohol abuse.293 While this enzyme was found in circulating exosomes from nonalcohol consuming patients, its amount is higher in people with AUD, which was additionally confirmed using experimental animal models.293 These studies were corroborated by unpublished studies from our laboratory showing elevated levels of CYP2E1 in alcohol-exposed hepatocyte-derived exosomes, as well as enhanced amounts of ADH and the lipid peroxidation markers, MDA and MAA. Since hepatocytes are the main cells that metabolize ingested ethanol, the transfer of ethanol-metabolizing enzymes with exosomes from hepatocytes to other organs may not only promote alcohol toxicity but may also induce detrimental effects in ethanol non-metabolizing organs.

Furthermore, the EVs containing viral RNAs may contribute to the transmission of HCV infection to healthy hepatocytes.147 Because HCV enhances exosome release from infected Huh 7.5.1cells,294 and because alcohol increases EVs release from hepatocytes,288 the spread of HCV in the liver with EVs will likely be more efficient in people with AUD. This transmission of viral RNAs/DNAs with exosomes is not unique for HCV infection. This is also the case for HBV infection,295,296 as well as for HIV infection in hepatocytes exposed to EtOH.297

Overall, EVs are becoming valuable tools for detecting cell-to-cell and interorgan communication after alcohol exposure.298 With further characterization, they will likely serve as essential diagnostic tools to characterize the varying pathologies that characterize the advancing stages in the spectrum of ALD. The scheme of EV-based interactions crucial for ALD development is presented in Figure6.

Macromolecule Transport - an overview (1)

Figure6. Alcohol-induced extracellular vesicles mediate cell-to-cell crosstalk in the liver. Alcohol exposure causes the release of extracellular vesicles (EVs) from parenchymal (hepatocytes) and nonparenchymal (Kupffer) liver cells. These EVs contain miRNAs, DNA, lipids, proteins, alcohol-metabolizing enzymes and viral RNAs/proteins (in virally infected livers). These cargoes are transmitted between hepatocytes and macrophages, which affect cell functions via EV-mediated crosstalk between donor and recipient cells.

ALD is a major cause of global disease burden and a leading cause of mortality. While many elements in ALD pathogenesis have been uncovered, there is still no FDA-approved therapy for this disease. Given the multifactorial nature of ALD development and progression, the multitude of disease modifiers, and the identification of potential new targets, it is conceivable that a multitherapeutic regimen may be needed to treat different stages in the spectrum of this disease.

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