Matrix Biology最新文献

{"title":"IGF-II regulates lysyl oxidase propeptide and mediates its effects in part via basic helix-loop-helix E40","authors":"Adegboyega Timothy Adewale,&nbsp;Shailza Sharma,&nbsp;Joe E. Mouawad,&nbsp;Xinh-Xinh Nguyen,&nbsp;Amy D. Bradshaw,&nbsp;Carol Feghali-Bostwick","doi":"10.1016/j.matbio.2024.06.002","DOIUrl":"10.1016/j.matbio.2024.06.002","url":null,"abstract":"<div><p>Pulmonary fibrosis (PF) is a clinically severe and commonly fatal complication of Systemic Sclerosis (SSc). Our group has previously reported profibrotic roles for Insulin-like Growth Factor II (IGF-II) and Lysyl Oxidase (LOX) in SSc-PF. We sought to identify downstream regulatory mediators of IGF-II. In the present work, we show that SSc lung tissues have higher baseline levels of the total (N-glycosylated/unglycosylated) LOX-Propeptide (LOX-PP) than control lung tissues. LOX-PP-mediated changes were consistent with the extracellular matrix (ECM) deregulation implicated in SSc-PF progression. Furthermore, Tolloid-like 1 (TLL1) and Bone Morphogenetic Protein 1 (BMP1), enzymes that can cleave ProLOX to release LOX-PP, were increased in SSc lung fibrosis and the bleomycin (BLM)-induced murine lung fibrosis model, respectively. In addition, IGF-II regulated the levels of ProLOX, active LOX, LOX-PP, BMP1, and isoforms of TLL1. The Class E Basic Helix-Loop-Helix protein 40 (BHLHE40) transcription factor localized to the nucleus in response to IGF-II. BHLHE40 silencing downregulated TLL1 isoforms and LOX-PP, and restored features of ECM deregulation triggered by IGF-II. Our findings indicate that IGF-II, BHLHE40, and LOX-PP may serve as targets of therapeutic intervention to halt SSc-PF progression.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"132 ","pages":"Pages 24-33"},"PeriodicalIF":4.5,"publicationDate":"2024-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141297184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular and epigenetic ex vivo profiling of testis cancer-associated fibroblasts and their interaction with germ cell tumor cells and macrophages","authors":"Alexa Stephan ,&nbsp;Jan-Henrik Suhrmann ,&nbsp;Margaretha A. Skowron ,&nbsp;Yue Che ,&nbsp;Gereon Poschmann ,&nbsp;Patrick Petzsch ,&nbsp;Catena Kresbach ,&nbsp;Wasco Wruck ,&nbsp;Pailin Pongratanakul ,&nbsp;James Adjaye ,&nbsp;Kai Stühler ,&nbsp;Karl Köhrer ,&nbsp;Ulrich Schüller ,&nbsp;Daniel Nettersheim","doi":"10.1016/j.matbio.2024.06.001","DOIUrl":"10.1016/j.matbio.2024.06.001","url":null,"abstract":"<div><p>Germ cell tumors (GCT) are the most common solid tumors in young men of age 15 - 40. In previous studies, we profiled the interaction of GCT cells with cells of the tumor microenvironment (TM), which showed that especially the 3D interaction of fibroblasts (FB) or macrophages with GCT cells influenced the growth behavior and cisplatin response as well as the transcriptome and secretome of the tumor cells, suggesting that the crosstalk of these cells with GCT cells is crucial for tumor progression and therapy outcome.</p><p>In this study, we shed light on the mechanisms of activation of cancer-associated fibroblasts (CAF) in the GCT setting and their effects on GCT cells lines and the monocyte cell line THP-1. <em>Ex vivo</em> cultures of GCT-derived CAF were established and characterized molecularly and epigenetically by performing DNA methylation arrays, RNA sequencing, and mass spectrometry-based secretome analysis.</p><p>We demonstrated that the activation state of CAF is influenced by their former prevailing tumor environment in which they have resided. Hereby, we postulate that seminoma (SE) and embryonal carcinoma (EC) activate CAF, while teratoma (TER) play only a minor role in CAF formation. In turn, CAF influence proliferation and the expression of cisplatin sensitivity-related factors in GCT cells lines as well as polarization of <em>in vitro</em>-induced macrophages by the identified effector molecules IGFBP1, LGALS3BP, LYVE1, and PTX3.</p><p>Our data suggests that the vital interaction of CAF with GCT cells and with macrophages has a huge influence on shaping the extracellular matrix as well as on recruitment of immune cells to the TM. In conclusion, therapeutically interfering with CAF and / or macrophages in addition to the standard therapy might slow-down progression of GCT and re-shaping of the TM to a tumor-promoting environment.</p><p>Significance: The interaction of CAF with GCT and macrophages considerably influences the microenvironment. Thus, therapeutically interfering with CAF might slow-down progression of GCT and re-shaping of the microenvironment to a tumor-promoting environment.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"132 ","pages":"Pages 10-23"},"PeriodicalIF":6.9,"publicationDate":"2024-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0945053X24000775/pdfft?md5=233b8097421e2225d8cf6fc3ee1b782b&pid=1-s2.0-S0945053X24000775-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141293904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ameloblastin and its multifunctionality in amelogenesis: A review","authors":"Natalie C. Kegulian ,&nbsp;Gayathri Visakan ,&nbsp;Rucha Arun Bapat,&nbsp;Janet Moradian-Oldak","doi":"10.1016/j.matbio.2024.05.007","DOIUrl":"10.1016/j.matbio.2024.05.007","url":null,"abstract":"<div><p>Extracellular matrix proteins play crucial roles in the formation of mineralized tissues like bone and teeth via multifunctional mechanisms. In tooth enamel, ameloblastin (Ambn) is one such multifunctional extracellular matrix protein implicated in cell signaling and polarity, cell adhesion to the developing enamel matrix, and stabilization of prismatic enamel morphology. To provide a perspective for Ambn structure and function, we begin this review by describing dental enamel and enamel formation (amelogenesis) followed by a description of enamel extracellular matrix. We then summarize the established domains and motifs in Ambn protein, human <em>amelogenesis imperfecta</em> cases, and genetically engineered mouse models involving mutated or null <em>Ambn.</em> We subsequently delineate <em>in silico, in vitro</em>, and <em>in vivo</em> evidence for the amphipathic helix in Ambn as a proposed cell-matrix adhesive and then more recent <em>in vitro</em> evidence for the multitargeting domain as the basis for dynamic interactions of Ambn with itself, amelogenin, and membranes. The multitargeting domain facilitates tuning between Ambn-membrane interactions and self/co-assembly and supports a likely overall role for Ambn as a matricellular protein. We anticipate that this review will enhance the understanding of multifunctional matrix proteins by consolidating diverse mechanisms through which Ambn contributes to enamel extracellular matrix mineralization.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"131 ","pages":"Pages 62-76"},"PeriodicalIF":6.9,"publicationDate":"2024-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141181124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sdc4 deletion perturbs intervertebral disc matrix homeostasis and promotes early osteopenia in the aging mouse spine","authors":"Kimheak Sao ,&nbsp;Makarand V. Risbud","doi":"10.1016/j.matbio.2024.05.006","DOIUrl":"10.1016/j.matbio.2024.05.006","url":null,"abstract":"<div><p>Syndecan 4 (SDC4), a cell surface heparan sulfate proteoglycan, is known to regulate matrix catabolism by nucleus pulposus cells in an inflammatory milieu. However, the role of SDC4 in the aging spine has never been explored. Here we analyzed the spinal phenotype of <em>Sdc4</em> global knockout (KO) mice as a function of age. Micro-computed tomography showed that <em>Sdc4</em> deletion severely reduced vertebral trabecular and cortical bone mass, and biomechanical properties of vertebrae were significantly altered in <em>Sdc4</em> KO mice. These changes in vertebral bone were likely due to elevated osteoclastic activity. The histological assessment showed subtle phenotypic changes in the intervertebral disc. Imaging-Fourier transform-infrared analyses showed a reduced relative ratio of mature collagen crosslinks in young adult nucleus pulposus (NP) and annulus fibrosus (AF) of KO compared to wildtype discs. Additionally, relative chondroitin sulfate levels increased in the NP compartment of the KO mice. Transcriptomic analysis of NP tissue using CompBio, an AI-based tool showed biological themes associated with prominent dysregulation of heparan sulfate GAG degradation, mitochondria metabolism, autophagy, endoplasmic reticulum (ER)-associated misfolded protein processes and ER to Golgi protein processing. Overall, this study highlights the important role of SDC4 in fine-tuning vertebral bone homeostasis and extracellular matrix homeostasis in the mouse intervertebral disc.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"131 ","pages":"Pages 46-61"},"PeriodicalIF":6.9,"publicationDate":"2024-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141162775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Collagen XVIII regulates extracellular matrix integrity in the developing nephrons and impacts nephron progenitor cell behavior","authors":"Mia M. Rinta-Jaskari ,&nbsp;Florence Naillat ,&nbsp;Heli J. Ruotsalainen ,&nbsp;Veli-Pekka Ronkainen ,&nbsp;Ritva Heljasvaara ,&nbsp;Saad U. Akram ,&nbsp;Valerio Izzi ,&nbsp;Ilkka Miinalainen ,&nbsp;Seppo J. Vainio ,&nbsp;Taina A. Pihlajaniemi","doi":"10.1016/j.matbio.2024.05.005","DOIUrl":"10.1016/j.matbio.2024.05.005","url":null,"abstract":"<div><p>Renal development is a complex process in which two major processes, tubular branching and nephron development, regulate each other reciprocally. Our previous findings have indicated that collagen XVIII (ColXVIII), an extracellular matrix protein, affects the renal branching morphogenesis. We investigate here the role of ColXVIII in nephron formation and the behavior of nephron progenitor cells (NPCs) using isoform-specific ColXVIII knockout mice. The results show that the short ColXVIII isoform predominates in the early epithelialized nephron structures whereas the two longer isoforms are expressed only in the later phases of glomerular formation. Meanwhile, electron microscopy showed that the ColXVIII mutant embryonic kidneys have ultrastructural defects at least from embryonic day 16.5 onwards. Similar structural defects had previously been observed in adult ColXVIII-deficient mice, indicating a congenital origin. The lack of ColXVIII led to a reduced NPC population in which changes in NPC proliferation and maintenance and in macrophage influx were perceived to play a role. The changes in NPC behavior in turn led to notably reduced overall nephron formation. In conclusion, the results show that ColXVIII has multiple roles in renal development, both in ureteric branching and in NPC behavior.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"131 ","pages":"Pages 30-45"},"PeriodicalIF":6.9,"publicationDate":"2024-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0945053X24000660/pdfft?md5=224053ebc87274accced0b682c6584ee&pid=1-s2.0-S0945053X24000660-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141093328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of amelogenin phosphorylation in regulating dental enamel formation","authors":"Claire M. Gabe ,&nbsp;Ai Thu Bui ,&nbsp;Lyudmila Lukashova ,&nbsp;Kostas Verdelis ,&nbsp;Brent Vasquez ,&nbsp;Elia Beniash ,&nbsp;Henry C. Margolis","doi":"10.1016/j.matbio.2024.05.004","DOIUrl":"10.1016/j.matbio.2024.05.004","url":null,"abstract":"<div><p>Amelogenin (AMELX), the predominant matrix protein in enamel formation, contains a singular phosphorylation site at Serine 16 (S16) that greatly enhances AMELX's capacity to stabilize amorphous calcium phosphate (ACP) and inhibit its transformation to apatitic enamel crystals. To explore the potential role of AMELX phosphorylation in vivo, we developed a knock-in (KI) mouse model in which AMELX phosphorylation is prevented by substituting S16 with Ala (A). As anticipated, AMELX^S16A KI mice displayed a severe phenotype characterized by weak hypoplastic enamel, absence of enamel rods, extensive ectopic calcifications, a greater rate of ACP transformation to apatitic crystals, and progressive cell pathology in enamel-forming cells (ameloblasts). In the present investigation, our focus was on understanding the mechanisms of action of phosphorylated AMELX in amelogenesis. We have hypothesized that the absence of AMELX phosphorylation would result in a loss of controlled mineralization during the secretory stage of amelogenesis, leading to an enhanced rate of enamel mineralization that causes enamel acidification due to excessive proton release. To test these hypotheses, we employed microcomputed tomography (µCT), colorimetric pH assessment, and Fourier Transform Infrared (FTIR) microspectroscopy of apical portions of mandibular incisors from 8-week old wildtype (WT) and KI mice. As hypothesized, µCT analyses demonstrated significantly higher rates of enamel mineral densification in KI mice during the secretory stage compared to the WT. Despite a greater rate of enamel densification, maximal KI enamel thickness increased at a significantly lower rate than that of the WT during the secretory stage of amelogenesis, reaching a thickness in mid-maturation that is approximately half that of the WT. pH assessments revealed a lower pH in secretory enamel in KI compared to WT mice, as hypothesized. FTIR findings further demonstrated that KI enamel is comprised of significantly greater amounts of acid phosphate compared to the WT, consistent with our pH assessments. Furthermore, FTIR microspectroscopy indicated a significantly higher mineral-to-organic ratio in KI enamel, as supported by µCT findings. Collectively, our current findings demonstrate that phosphorylated AMELX plays crucial mechanistic roles in regulating the rate of enamel mineral formation, and in maintaining physico-chemical homeostasis and the enamel growth pattern during early stages of amelogenesis.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"131 ","pages":"Pages 17-29"},"PeriodicalIF":6.9,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140959746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined genetic-pharmacologic inactivation of tightly linked ADAMTS proteases in temporally specific windows uncovers distinct roles for versican proteolysis and glypican-6 in cardiac development","authors":"Timothy J. Mead ,&nbsp;Sumit Bhutada ,&nbsp;Simon J. Foulcer ,&nbsp;Niccolò Peruzzi ,&nbsp;Courtney M. Nelson ,&nbsp;Deborah E. Seifert ,&nbsp;Jonathan Larkin ,&nbsp;Karin Tran-Lundmark ,&nbsp;Jorge Filmus ,&nbsp;Suneel S. Apte","doi":"10.1016/j.matbio.2024.05.003","DOIUrl":"10.1016/j.matbio.2024.05.003","url":null,"abstract":"<div><p>Extracellular matrix remodeling mechanisms are understudied in cardiac development and congenital heart defects. We show that matrix-degrading metalloproteases ADAMTS1 and ADAMTS5, are extensively co-expressed during mouse cardiac development. The mouse mutants of each gene have mild cardiac anomalies, however, their combined genetic inactivation to elicit cooperative roles is precluded by tight gene linkage. Therefore, we coupled <em>Adamts1</em> inactivation with pharmacologic ADAMTS5 blockade to uncover stage-specific cooperative roles and investigated their potential substrates in mouse cardiac development. ADAMTS5 blockade was achieved in <em>Adamts1</em> null mouse embryos using an activity-blocking monoclonal antibody during distinct developmental windows spanning myocardial compaction or cardiac septation and outflow tract rotation. Synchrotron imaging, RNA in situ hybridization, immunofluorescence microscopy and electron microscopy were used to determine the impact on cardiac development and compared to <em>Gpc6</em> and ADAMTS-cleavage resistant versican mutants. Mass spectrometry-based N-terminomics was used to seek relevant substrates. Combined inactivation of ADAMTS1 and ADAMTS5 prior to 12.5 days of gestation led to dramatic accumulation of versican-rich cardiac jelly and inhibited formation of compact and trabecular myocardium, which was also observed in mice with ADAMTS cleavage-resistant versican. Combined inactivation after 12.5 days impaired outflow tract development and ventricular septal closure, generating a tetralogy of Fallot-like defect. N-terminomics of combined ADAMTS knockout and control hearts identified a cleaved glypican-6 peptide only in the controls. ADAMTS1 and ADAMTS5 expression in cells was associated with specific glypican-6 cleavages. Paradoxically, combined ADAMTS1 and ADAMTS5 inactivation reduced cardiac glypican-6 and outflow tract <em>Gpc6</em> transcription. Notably, <em>Gpc6</em>^−/− hearts demonstrated similar rotational defects as combined ADAMTS inactivated hearts and both had reduced hedgehog signaling. Thus, versican proteolysis in cardiac jelly at the canonical Glu⁴⁴¹-Ala⁴⁴² site is cooperatively mediated by ADAMTS1 and ADAMTS5 and required for proper ventricular cardiomyogenesis, whereas, reduced glypican-6 after combined ADAMTS inactivation impairs hedgehog signaling, leading to outflow tract malrotation.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"131 ","pages":"Pages 1-16"},"PeriodicalIF":6.9,"publicationDate":"2024-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0945053X24000647/pdfft?md5=b11e9a1d15b013efc4ad3ad6735b73f4&pid=1-s2.0-S0945053X24000647-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140946351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LPA-induced expression of CCN2 in muscular fibro/adipogenic progenitors (FAPs): Unraveling cellular communication networks","authors":"Adriana Córdova-Casanova ,&nbsp;Meilyn Cruz-Soca ,&nbsp;Felipe S. Gallardo ,&nbsp;Jennifer Faundez-Contreras ,&nbsp;Alexia Bock-Pereda ,&nbsp;Jerold Chun ,&nbsp;Carlos P. Vio ,&nbsp;Juan Carlos Casar ,&nbsp;Enrique Brandan","doi":"10.1016/j.matbio.2024.05.001","DOIUrl":"10.1016/j.matbio.2024.05.001","url":null,"abstract":"<div><p>Cellular Communication Network Factor 2, CCN2, is a profibrotic cytokine implicated in physiological and pathological processes in mammals. The expression of CCN2 is markedly increased in dystrophic muscles. Interestingly, diminishing CCN2 genetically or inhibiting its function improves the phenotypes of chronic muscular fibrosis in rodent models. Elucidating the cell-specific mechanisms behind the induction of CCN2 is a fundamental step in understanding its relevance in muscular dystrophies. Here, we show that the small lipids LPA and 2S-OMPT induce CCN2 expression in fibro/adipogenic progenitors (FAPs) through the activation of the LPA₁ receptor and, to a lower extent, by also the LPA₆ receptor. These cells show a stronger induction than myoblasts or myotubes. We show that the LPA/LPARs axis requires ROCK kinase activity and organized actin cytoskeleton upstream of YAP/TAZ signaling effectors to upregulate CCN2 levels, suggesting that mechanical signals are part of the mechanism behind this process. In conclusion, we explored the role of the LPA/LPAR axis on CCN2 expression, showing a strong cytoskeletal-dependent response in muscular FAPs.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"130 ","pages":"Pages 36-46"},"PeriodicalIF":6.9,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140899651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transglutaminase-mediated stiffening of the glomerular basement membrane mitigates pressure-induced reductions in molecular sieving coefficient by reducing compression","authors":"Dan Wang,&nbsp;Nicholas Ferrell","doi":"10.1016/j.matbio.2024.05.002","DOIUrl":"10.1016/j.matbio.2024.05.002","url":null,"abstract":"<div><p>Proteinuria, the presence of high molecular weight proteins in the urine, is a primary indicator of chronic kidney disease. Proteinuria results from increased molecular permeability of the glomerular filtration barrier combined with saturation or defects in tubular protein reabsorption. Any solute that passes into the glomerular filtrate traverses the glomerular endothelium, the glomerular basement membrane, and the podocyte slit diaphragm. Damage to any layer of the filter has reciprocal effects on other layers to increase glomerular permeability. The GBM is thought to act as a compressible ultrafilter that has increased molecular selectivity with increased pressure due to compression that reduced the porosity of the GBM with increased pressure. In multiple forms of chronic kidney disease, crosslinking enzymes are upregulated and may act to increase GBM stiffness. Here we show that enzymatically crosslinking porcine GBM with transglutaminase increases the stiffness of the GBM and mitigates pressure-dependent reductions in molecular sieving coefficient. This was modeled mathematically using a modified membrane transport model accounting for GBM compression. Changes in the mechanical properties of the GBM may contribute to proteinuria through pressure-dependent effects on GBM porosity.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"130 ","pages":"Pages 47-55"},"PeriodicalIF":6.9,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0945053X24000635/pdfft?md5=ca3c58b7bcee7290a259da192b79305e&pid=1-s2.0-S0945053X24000635-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140899656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Fibrolamellar carcinomas–growth arrested by paracrine signals complexed with synthesized 3-O sulfated heparan sulfate oligosaccharides” [Matrix Biology 121(August 2023), 194–216]","authors":"Wencheng Zhang ,&nbsp;Yongmei Xu ,&nbsp;Xicheng Wang ,&nbsp;Tsunekazu Oikawa ,&nbsp;Guowei Su ,&nbsp;Eliane Wauthier ,&nbsp;Guoxiu Wu ,&nbsp;Praveen Sethupathy ,&nbsp;Zhiying He ,&nbsp;Jian Liu ,&nbsp;Lola M. Reid","doi":"10.1016/j.matbio.2024.03.004","DOIUrl":"https://doi.org/10.1016/j.matbio.2024.03.004","url":null,"abstract":"","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"129 ","pages":"Page 59"},"PeriodicalIF":6.9,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0945053X24000416/pdfft?md5=8ab4e18576f9e202f1b1977a9ab70398&pid=1-s2.0-S0945053X24000416-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140842668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}