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The Role of Light and Electromagnetic Fields in Maintaining Vascular Health
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
The basement membrane is the thin delicate membrane made up of protein fibers and glycosaminoglycans separating the epithelium from the underlying tissues. The dense layer closer to the connective tissue is called the lamina densa. It contains multiple collagen IV fibers coated with the heparan-sulfate rich proteoglycan, perlecan [16]. Perlecan also serves as a barrier between the circulating blood and the surrounding tissue [17]. It maintains the integrity of microvessels [18], and white blood cells must cross a perlecan barrier in order to extravasate into the surrounding tissues.
Structural and Functional Consequences of Streptozotocin-Induced Diabetes on the Kidney
Published in John H. McNeill, Experimental Models of Diabetes, 2018
Kumar Sharma, Dong Cheol Han, András Mogyorósi, Fuad N. Ziyadeh
The exact biochemical and ultrastructural basis for the thickening of GBM and the increased permeability for macromolecules across the filtration barrier of the glomerular capillary wall remain only partly understood. A heterogeneous population of collagenous and noncollagenous proteins has been identified in the GBM. The most important constituent in quantitative terms is Type IV collagen. Other macromolecules include proteoglycans, namely, heparan sulfate proteoglycan (HSPG or perlecan) and structural glycoproteins (laminin, nidogen/entactin, and perhaps fibronectin).73 It has been suggested that increased synthesis and/or decreased degradation of collagens and laminins are responsible for increased GBM thickness.75 Hirose et al.78 demonstrated progressive thickening of GBM in untreated STZ diabetic rats during 18 months of diabetes. Similar results were found in moderately hyperglycemic diabetic rats after 6 months of diabetes.77 The thickness of GBM was reversible by strict blood glucose control with insulin.77 Diffuse thickening of the GBM was highly variable from one capillary loop to another.91 In a recent paper, Brees et al.92 found no change in the content of Type IV collagen and nidogen/entactin but a significant increase in laminin and fibronectin in GBM extracts from rats after 3 months of STZ-induced diabetes.
Immunohistochemical Characterization of Extracellular Matrix in Tumor Tissues
Published in Róza Ádány, Tumor Matrix Biology, 2017
Perlecan, basement membrane heparan sulfate proteoglycan, can interact with several other basement membrane macromolecules, including laminin and type IV collagen.14–16 It also has been demonstrated that basement membrane heparan sulfate proteoglycan isolated from Engelbreth-Holm-Swarm (EHS) tumor binds to laminin, type IV collagen, and fibronectin by its heparan sulfate chains and to entactin (nidogen) through its protein core.17
Spatial composition and turnover of the main molecules in the adult glomerular basement membrane
Published in Tissue Barriers, 2023
David W. Smith, Azin Azadi, Chang-Joon Lee, Bruce S. Gardiner
There is information on the amount of HS attached to the proteoglycans, though these data are mainly from chicks, with some human data for perlecan. Chick brain agrin core protein is about 220 kDa, while the intact agrin proteoglycan is reported to be in excess of 400 kDa.48 We estimate that about 200 kDa of HS is attached to intact GBM agrin. Human perlecan core protein is reported to be 467 kDa, while intact perlecan has 3 HS side chains and possibly a chondroitin sulfate side chain, with a total weight of up to 750 kDa.49 Intact GBM perlecan has about 200 kDa of HS attached to it.49 We base this estimate on the following. For the collagen XVIII found in the chick embryo, it is reported the collagen XVIII ‘core chain protein’ is 180 kDa, which has 120 kDa of HS attached to it.50 We treble values for the core chain protein of collagen XVIII to approximately estimate a value for the homotrimer of intact collagen XVIII (i.e., we assume 300 kDa of HS is attached to collagen XVIII).
GRP75 as a functional element of cholix transcytosis
Published in Tissue Barriers, 2023
Keyi Liu, Tom Hunter, Alistair Taverner, Kevin Yin, Julia MacKay, Kate Colebrook, Morgan Correia, Amandine Rapp, Randall J. Mrsny
Chx uses an apical endocytosis event that involves TMEM132A and EEA1 to deliver it to early endosomes containing GRP75 in the apical compartment of enterocytes. Previous studies suggested a role for perlecan in its apical endocytosis and early trafficking,10 with the current studies suggesting that this may involve a direct interaction with GRP75. Studies with non-polarized cells have demonstrated that perlecan can mediate a slower-than-expected pathway of internalization and lysosomal delivery of a variety of ligands.28 Specific interactions between perlecan and cell surface receptors, however, can also affect the fate of associated ligands following endocytosis, deviating their fate from the default outcome of routing to lysosomes.29 In this polarized cell system, perlecan and GRP75 may function in routing Chx away from the default lysosomal degradation pathway,30 facilitating the privileged pathway concept for the A→B transcytosis pathway hijacked by this exotoxin where it fails to enter lysosomes.16 As GRP75 can interact with GRP9431 and GRP94 appears to avoid lysosomes,32the mechanism used by Chx to avoid a lysosomal fate may involve the function of GRP75 binding partners.
Maternal serum perlecan levels in women with preeclampsia
Published in Hypertension in Pregnancy, 2020
Murat Akbas, Faik Mumtaz Koyuncu, Burcu Artunc-Ulkumen, Fatma Taneli, Habib Ozdemir
Although the pathophysiology underlying the disease has been partially elucidated, the definitive mechanisms of preeclampsia remain unknown. Data in the literature have supported the classification of preeclampsia into two distinct entities as early-onset preeclampsia (EOP) and late-onset preeclampsia (LOP). The pathophysiological features and clinical course differ between two forms (7). EOP is thought to be the consequence of a deficiency in spiral artery remodeling and inadequate trophoblastic invasion that is characterized with angiogenic and anti-angiogenic molecule imbalance (8,9). EOP is associated with decreased placental volume, abnormal Doppler findings and intrauterine growth restriction (10). Whereas, the under perfusion of the overgrown placenta associated with an underlying maternal constitutional disorder is responsible for the development of LOP (11). LOP is usually associated with larger placental volume, normal Doppler findings and normal fetal growth (7). Perlecan is a large proteoglycan divided into five distinct domains with attachment sites for three heparan sulfate chains that interact extracellular matrix components and cell-surface molecules to maintain the endothelial function (12,13). Perlecan is abundant in the basement membrane where it helps to maintain the endothelial barrier function and vascular homeostasis (14). Also, perlecan was found to be upregulated in response to arterial injury in an animal model but was downregulated in human atherosclerotic lesions (15,16). Furthermore, perlecan depicts an inhibitor role on autophagy which may contribute to the pathophysiology of preeclampsia (17,18).