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Endorepellin evoked mitochondrial depolarization in endothelial cells via a specific interaction between its two proximal LG1/2 domains and VEGFR2.
Data provide evidence for the roles of HSPG2 in controlling/modulating fibrogenesis, promoting tissue repair whilst limiting damaging fibrosis even though many of the tissue repair activities can also contribute to fibrogenesis if not resolved on time. Its anti-fibrotic activities are mediated through modulating cell adhesion, proliferation and migration of key inflammatory and ECM producing cells. [review]
Molecular analysis results revealed a novel homozygous variant in the HSPG2 gene (MIM 142461), NM_005529.6(HSPG2):c.4029 + 1G>A, consistent with a diagnosis of Dyssegmental dysplasia, Silverman-Handmaker type.
The results of the present study suggested that the compound heterozygous mutations in HSPG2 may be responsible the induction of Schwartz-Jampel syndrome type 1 (SJS1), and demonstrated the genotypephenotype associations between mutations in the HSPG2 gene and clinical characteristics of SJS1
The differential immunoexpression of perlecan and biglycan in these types of ameloblastomas suggests their participation in the developmental process of these tumors.
The Mechanistic studies showed that CSPG4 bound to perlecan via hydrophobic protein-protein interactions involving multiple sites on perlecan including the C-terminal region.
The results indicate that increase of heparan sulfate content and up-regulation of perlecan/HSPG2 expression in glioblastoma tissues contribute to tumour development through the transformation of brain extracellular matrix into tumour microenvironment, and represent negative prognostic factors for glioblastoma progression.
Mutations in this gene are responsible for the allelic Skeletal Dysplasias Schwartz-Jampel syndrome type 1 and the Silverman-Handmaker type of Dyssegmental Dysplasia, both of which are autosomal recessive.
Perlecan functions in autophagy and angiogenesis where its proangiogenesis activity is counteracted by endorepellin, the C-terminal fragment of perlecan, in these cellular and morphogenic events. (Review)
We found that perlecan expression decreased during chronological skin aging. Our in vitro studies revealed reduced perlecan transcript levels in aged keratinocytes. Perlecan down-regulation in cultured keratinocytes caused depletion of the cell population that expressed keratin 15.Finally, we found defects in keratin 15 expression in the epidermis of aging skin.
Putative stem cell populations associated with hair bulbs, humeral perichondrium, humeral and ulnar rudiment stromal/perivascular tissues expressed the Chondroitin sulfate motifs 4C3, 7D4, and 3B3[-] along with perlecan in close association but not colocalized.
autophagy is a novel mechanism by which endorepellin promotes angiostasis independent of nutrient deprivation.
Heterozygous variants in HSPG2 regulate the ATP2B4 expression via a variety of transcription factors including GATA1, RFX1 and MAZ.
the HSPG2-rs3767140 might be associated with the decreased fasting plasma glucose and LDL-C and with the increased HDL-C in diabetics.
Together, perlecan fragments in sera and MMP-7 in tissues of Prostate cancer patients are measures of invasive Prostate cancer.
Results show that perlecan has physical properties that would allow it to act as a strong but elastic tether in the lacunar canalicular system of cortical bone.
We were able to identify perlecan as the most likely candidate for the major estrogen-binding protein in the follicular fluid.
Knockdown of agrin and perlecan promoted a decrease on cell migration and adhesion, and on resistance of cells to cisplatin.
As five of the seven missense mutations in Schwartz-Jampel syndrome affect domain III of perlecan, domain III is likely to be essential for secretion of perlecan into the extracellular space.
Rare variants in the HSPG2 gene potentially contribute to the idiopathic scoliosis phenotype in a subset of patients with idiopathic scoliosis
Nidogen-1 and nidogen-2 mRNAs were highly expressed in keratocytes, whereas perlecan was highly expressed in myofibroblasts.
RUS3108 is a novel perlecan-inducing compound which may prevent in-stent restenosis.
Perlecan is a defining factor in both the biochemical and biomechanical properties of the pericellular matrix.
Confocal laser scanning microscopy co-localised perlecan with type VI collagen as pericellular components of intervertebral disc (IVD) cells and translamellar cross-bridges in ovine and murine IVDs.
Perlecan knockdown altered matrix organization and significantly decreased the stiffness of both chondrocytes and interstitial matrix as a function of age and genotype.
Perlecan is required for the chondrogenic and adipogenic differentiation from SMCs via its regulation of the Sox9 and PPARgamma gene expression, but not for osteogenic differentiation via Runx2
The reduced deposition of TGF-beta1 observed in the present study would be expected to impact detrimentally on the remodelling and healing capacity of skin in mutant mice compounding on the poor wound-healing properties already reported for perlecan exon 3 null mice due to an inability to signal with FGF-2 and promote angiogenic repair processes.
Hspg2 inhibits autophagy to maintain muscle homeostasis in mouse soleus muscle.
Perlecan HS has significant roles in directing the development of posttraumatic OA, potentially via the alteration of FGF/HS/FGFR signaling.
An in situ hybridization study of perlecan, DMP1, and MEPE in developing condylar cartilage of the fetal mouse mandible and limb bud cartilage.
LG3, through interactions with alpha2beta1 integrins on recipient-derived cells leading to activation of ERK1/2 and increased migration, favors myointimal thickening
Corneal epithelial cells require HS for maintaining corneal homeostasis, and the loss of epithelial HS leads to both impaired wound healing and impaired corneal stratification
Perlecan binds the clustering molecule gliomedin and enhances clustering of node of Ranvier components.
perlecan deficiency alters cartilage matrix patterning and, as we now show, coordinately influences bone formation and calcification
applied a fluorescent technique to older mice expressing or deficient for perlecan/HSPG2, a large heparan-sulfate proteoglycan normally secreted in osteocytic PCM
[review] Perlecan domain V is present acutely and chronically after ischemic stroke and could have a role in acute neuroprotection and chronic neurorepair at the site of stroke brain injury.
Synovial perlecan plays an important role in osteophyte development in osteoarthritis.
Perlecan supports the maintenance of brain and skin subendothelial basement membranes and promotes vasculo- and angiogenesis by modulating FGF-2 function
The neuroprotective effects of perlecan domain V on astrocytes under physiological and pathological situations are studied in both in vitro and in vivo models.
Report immunolocalization of fibrillin-1/perlecan in HS-deficient hspg2 exon 3 null mutant mouse intervertebral disc.
study found that while release of pre-synthesized perlecan causes an increase in LG3 levels during oxygen-glucose deprivation in fetal cortical neurons (FCN), it is the increased de novo synthesis of perlecan in FCN which may be responsible for increased LG3 levels during reperfusion
Cartilage perlecan promoted activation of VEGF/VEGFR by binding to the VEGFR of endothelial cells.
Perlecan plays a role in Schwann cell growth and structure during development.
Blocking of perlecan by anti-perlecan antiserum inhibited the migration of vascular endothelial cells (VECs) and bone marrow-derived mesenchymal stem cells, and exogenous perlecan added to the culture medium promoted the migration of these cell types.
Hyperglycemia-induced structural changes in perlecan may result in a subendothelial matrix that is more favorable to retention of monocytes. 2 forms of perlecan exist in BAEC SEM, 1 with HS chains only and 1 with both HS and CS/DS chains.
results suggest that perlecan made by growth plate chondrocytes is a low affinity receptor for FGF-2 and acts to sequester FGF-2 away from the high affinity receptor
data show that growth plate perlecan binds to FGF-2 by its heparan sulfate chains but can only deliver FGF-2 to FGF receptors when its chondroitin sulfate chains are removed.
This gene encodes the perlecan protein, which consists of a core protein to which three long chains of glycosaminoglycans (heparan sulfate or chondroitin sulfate) are attached. The perlecan protein is a large multidomain proteoglycan that binds to and cross-links many extracellular matrix components and cell-surface molecules. It has been shown that this protein interacts with laminin, prolargin, collagen type IV, FGFBP1, FBLN2, FGF7 and Transthyretin, etc. and plays essential roles in multiple biological activities. Perlecan is a key component of the vascular extracellular matrix, where it helps to maintain the endothelial barrier function. It is a potent inhibitor of smooth muscle cell proliferation and is thus thought to help maintain vascular homeostasis. It can also promote growth factor (e.g., FGF2) activity and thus stimulate endothelial growth and re-generation. It is a major component of basement membranes, where it is involved in the stabilization of other molecules as well as being involved with glomerular permeability to macromolecules and cell adhesion. Mutations in this gene cause Schwartz-Jampel syndrome type 1, Silverman-Handmaker type of dyssegmental dysplasia, and Tardive dyskinesia.
basement membrane-specific heparan sulfate proteoglycan core protein
, endorepellin (domain V region)
, perlecan proteoglycan
, heparan sulfate proteoglycan 2
, basement membrane-specific heparan sulfate proteoglycan core protein-like
, perlecan (heparan sulfate proteoglycan 2)