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Tenascin integrin

Susobhan Sarkar, Reza Mirzaei, Franz J Zemp, Wei Wu, Donna L Senger, Stephen M Robbins, V Wee Yong
Elevated NOTCH signaling is implicated in tumorigenesis. The brain tumor- initiating cells (BTICs) present in malignant glioma exhibit elevated NOTCH activity but the mechanism of this activation is unknown. Here, we provide evidence that tenascin-C (TNC), an extracellular matrix protein prominent in malignant glioma, increases NOTCH activity in BTICs to promote their growth. We demonstrate the proximal localization of TNC and BTICs in human glioblastoma specimens, and in the brains of mice implanted with human BTIC intracranial xenografts...
April 17, 2017: Cancer Research
Keiichi Koshizuka, Nijiro Nohata, Toyoyuki Hanazawa, Naoko Kikkawa, Takayuki Arai, Atsushi Okato, Ichiro Fukumoto, Koji Katada, Yoshitaka Okamoto, Naohiko Seki
We adopted into RNA-sequencing technologies to construct the microRNA (miRNA) expression signature of head and neck squamous cell carcinoma (HNSCC). Our signature revealed that a total of 160 miRNAs (44 upregulated and 116 downregulated) were aberrantly expressed in cancer tissues. Expression of miR-150-5p (guide strand miRNA) and miR-150-3p (passenger strand miRNA) were significantly silenced in cancer tissues, suggesting both miRNAs act as antitumor miRNAs in HNSCC cells. Ectopic expression of mature miRNAs, miR-150-5p and miR-150-3p inhibited cancer cell aggressiveness...
March 17, 2017: Oncotarget
Menghon Cheah, Melissa R Andrews
Axon regeneration in the CNS is largely unsuccessful due to excess inhibitory extrinsic factors within lesion sites together with an intrinsic inability of neurons to regrow following injury. Recent work demonstrates that forced expression of certain neuronal transmembrane receptors can recapitulate neuronal growth resulting in successful growth within and through inhibitory lesion environments. More specifically, neuronal expression of integrin receptors such as alpha9beta1 integrin which binds the extracellular matrix glycoprotein tenascin-C, trk receptors such as trkB which binds the neurotrophic factor BDNF, and receptor PTPσ which binds chondroitin sulphate proteoglycans, have all been show to significantly enhance regeneration of injured axons...
December 2016: Neural Regeneration Research
Hiroe Toba, Presley L Cannon, Andriy Yabluchanskiy, Rugmani Padmanabhan Iyer, Jeanine D'Armiento, Merry L Lindsey
Advancing age is an independent risk factor for cardiovascular disease. Matrix metalloproteinase-9 (MMP-9) is secreted by macrophages and robustly increases in the left ventricle (LV) with age. The present study investigated the effect of MMP-9 overexpression in macrophages on cardiac aging. We compared 16- to 21-mo-old C57BL/6J wild-type (WT) and transgenic (TG) male and female mice (n = 15-20/group). MMP-9 overexpression amplified the hypertrophic response to aging, as evidenced by increased LV wall thickness and myocyte cross-sectional areas (P < 0...
March 1, 2017: American Journal of Physiology. Heart and Circulatory Physiology
J W Fawcett
Axon regeneration in the CNS is blocked by inhibitory molecules in the environment and by a developmental loss of regenerative potential in CNS axons. Axon growth is a specialized form of cell migration, and for any cell to migrate there must be an adhesion molecule at the growth tip that recognizes a ligand in the environment, and which is linked to signaling and cytoskeletal mechanisms. The reasons for this loss of regenerative ability in CNS axons are several, but important contributors are the developmental loss of integrins that recognize ligands in the mature CNS environment, and selective trafficking of integrins and other molecules to exclude them from axons and direct them to dendrites...
February 2017: Eye
Yoshiyuki Kobayashi, Shigeo Yoshida, Yedi Zhou, Takahito Nakama, Keijiro Ishikawa, Yuki Kubo, Mitsuru Arima, Shintaro Nakao, Toshio Hisatomi, Yasuhiro Ikeda, Akira Matsuda, Koh-Hei Sonoda, Tatsuro Ishibashi
Tenascin-C is expressed in choroidal neovascular (CNV) membranes in eyes with age-related macular degeneration (AMD). However, its role in the pathogenesis of CNV remains to be elucidated. Here we investigated the role of tenascin-C in CNV formation. In immunofluorescence analyses, tenascin-C co-stained with α-SMA, pan-cytokeratin, CD31, CD34, and integrin αV in the CNV membranes of patients with AMD and a mouse model of laser-induced CNV. A marked increase in the expression of tenascin-C mRNA and protein was observed 3 days after laser photocoagulation in the mouse CNV model...
September 26, 2016: Laboratory Investigation; a Journal of Technical Methods and Pathology
Haiyan Fu, Yuan Tian, Lili Zhou, Dong Zhou, Roderick J Tan, Donna B Stolz, Youhua Liu
Kidney fibrosis initiates at certain focal sites in which the fibrogenic niche provides a specialized microenvironment that facilitates fibroblast activation and proliferation. However, the molecular identity of these fibrogenic niches is poorly characterized. Here, we determined whether tenascin-C (TNC), an extracellular matrix glycoprotein, is a component of the fibrogenic niche in kidney fibrosis. In vivo, TNC expression increased rapidly in kidneys subjected to unilateral ureteral obstruction or ischemia/reperfusion injury and predominantly localized at the foci rich in fibroblasts in renal interstitium...
March 2017: Journal of the American Society of Nephrology: JASN
Ravi Thakur, Durga Prasad Mishra
Matricellular proteins (MCPs) are the non-structural extracellular matrix (ECM) proteins with various regulatory functions. MCPs are critical regulators of ECM homeostasis and are often found dysregulated in various malignancies. They interact with various proteins like ECM structural proteins, integrins, growth factor receptors and growth factors to modulate their availability and activity. Cancer-supporting MCPs are known to induce proliferation, migration and invasion of cancer cells. MCPs also support cancer stem (like) cell growth and induce a drug-resistant state...
December 2016: Pharmacology & Therapeutics
Melissa R Andrews, Sara Soleman, Menghon Cheah, David A Tumbarello, Matthew R J Mason, Elizabeth Moloney, Joost Verhaagen, Jean-Charles Bensadoun, Bernard Schneider, Patrick Aebischer, James W Fawcett
The regenerative ability of CNS axons decreases with age, however, this ability remains largely intact in PNS axons throughout adulthood. These differences are likely to correspond with age-related silencing of proteins necessary for axon growth and elongation. In previous studies, it has been shown that reintroduction of the α9 integrin subunit (tenascin-C receptor, α9) that is downregulated in adult CNS can improve neurite outgrowth and sensory axon regeneration after a dorsal rhizotomy or a dorsal column crush spinal cord lesion...
July 2016: ENeuro
Nicola Chiarelli, Giulia Carini, Nicoletta Zoppi, Chiara Dordoni, Marco Ritelli, Marina Venturini, Marco Castori, Marina Colombi
Joint hypermobility syndrome/Ehlers-Danlos syndrome hypermobility type (JHS/EDS-HT), is likely the most common systemic heritable connective tissue disorder, and is mostly recognized by generalized joint hypermobility, joint instability complications, minor skin changes and a wide range of satellite features. JHS/EDS-HT is considered an autosomal dominant trait but is still without a defined molecular basis. The absence of (a) causative gene(s) for JHS/EDS-HT is likely attributable to marked genetic heterogeneity and/or interaction of multiple loci...
2016: PloS One
Edward Helal-Neto, Renata M Brandão-Costa, Roberta Saldanha-Gama, Cristiane Ribeiro-Pereira, Victor Midlej, Marlene Benchimol, Verônica Morandi, Christina Barja-Fidalgo
The unique composition of tumor-produced extracellular matrix (ECM) can be a determining factor in changing the profile of endothelial cells in the tumor microenvironment. As the main receptor for ECM proteins, integrins can activate a series of signaling pathways related to cell adhesion, migration, and differentiation of endothelial cells that interact with ECM proteins. We studied the direct impact of the decellularized ECM produced by a highly metastatic human melanoma cell line (MV3) on the activation of endothelial cells and identified the intracellular signaling pathways associated with cell differentiation...
November 2016: Journal of Cellular Physiology
Menghon Cheah, Melissa R Andrews, Daniel J Chew, Elizabeth B Moloney, Joost Verhaagen, Reinhard Fässler, James W Fawcett
UNLABELLED: After CNS injury, axon regeneration is blocked by an inhibitory environment consisting of the highly upregulated tenascin-C and chondroitin sulfate proteoglycans (CSPGs). Tenascin-C promotes growth of axons if they express a tenascin-binding integrin, particularly α9β1. Additionally, integrins can be inactivated by CSPGs, and this inhibition can be overcome by the presence of a β1-binding integrin activator, kindlin-1. We examined the synergistic effect of α9 integrin and kindlin-1 on sensory axon regeneration in adult rat spinal cord after dorsal root crush and adeno-associated virus transgene expression in dorsal root ganglia...
July 6, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Rainer Kluger, Joerg Burgstaller, Claus Vogl, Gottfried Brem, Michal Skultety, Simone Mueller
Evidence for a heritable predisposition to rotator cuff tears (RCTs) is growing. Unrelated Caucasian individuals with surgically diagnosed full thickness RCTs (cases) and elderly Caucasian controls with intact rotator cuffs were screened for differences at the candidate genes: TNC, Col5A1, TIMP-1, MMP-1, MMP-2, MMP-3, MMP-9, and MMP-13. A first cohort (59 cases; 32 controls) was genotyped with the Sequenom MassARRAY iPLEX system. Of 142 SNPs within about 67 kbp of the TNC gene, 30 were tested for differences in proportions between cases and controls...
June 1, 2016: Journal of Orthopaedic Research: Official Publication of the Orthopaedic Research Society
Yoshiyuki Kobayashi, Shigeo Yoshida, Yedi Zhou, Takahito Nakama, Keijiro Ishikawa, Mitsuru Arima, Shintaro Nakao, Yukio Sassa, Atsunobu Takeda, Toshio Hisatomi, Yasuhiro Ikeda, Akira Matsuda, Koh-Hei Sonoda, Tatsuro Ishibashi
PURPOSE: We previously demonstrated that tenascin-C was highly expressed in the fibrovascular membranes (FVMs) of patients with proliferative diabetic retinopathy (PDR). However, its role in the pathogenesis of FVMs has not been determined. The purpose of this study was to investigate what role tenascin-C plays in the formation and angiogenesis of FVMs. METHODS: The level of tenascin-C was determined by sandwich enzyme-linked immunosorbent assay in the vitreous samples collected from patients with PDR and with a macular hole as control...
2016: Molecular Vision
Eric J Berns, Zaida Álvarez, Joshua E Goldberger, Job Boekhoven, John A Kessler, H Georg Kuhn, Samuel I Stupp
UNLABELLED: Biomimetic materials that display natural bioactive signals derived from extracellular matrix molecules like laminin and fibronectin hold promise for promoting regeneration of the nervous system. In this work, we investigated a biomimetic peptide amphiphile (PA) presenting a peptide derived from the extracellular glycoprotein tenascin-C, known to promote neurite outgrowth through interaction with β1 integrin. The tenascin-C mimetic PA (TN-C PA) was found to self-assemble into supramolecular nanofibers and was incorporated through co-assembly into PA gels formed by highly aligned nanofibers...
June 2016: Acta Biomaterialia
Jian-Cang Ma, Xin Huang, Ya-Wei Shen, Chen Zheng, Qing-Hua Su, Jin-Kai Xu, Jun Zhao
Tenascin-C (TN-C) is an extracellular matrix glycoprotein markedly upregulated during liver fibrosis. The study is performed to explore the role of TN-C during the growth and activation of hepatic stellate cells (HSCs). We found that TN-C was accumulated accompanying with the HSC activation. Our data on cell migration assay revealed that the rTN-C treatment enhanced HSC migration in a dose- and time-dependent manner, but did not influence their proliferation. HSCs transfected with pTARGET-TN-C overexpression vector displayed increased the type I collagen (Col I) production...
August 2016: Bioscience, Biotechnology, and Biochemistry
Juxing Chen, Guillermo Tellez, Jeffery Escobar
Footpad dermatitis (FPD) is a type of skin inflammation that causes necrotic lesions on the plantar surface of the footpads in commercial poultry, with significant animal welfare, and economic implications. To identify biomarkers for FPD development and wound healing, a battery cage trial was conducted in which a paper sheet was put on the bottom of cages to hold feces to induce FPD of broilers. Day-of-hatch Ross 308 male broiler chicks were fed a corn-soybean meal diet and assigned to 3 treatments with 8 cages per treatment and 11 birds per cage...
2016: Frontiers in Cellular and Infection Microbiology
Anna Afasizheva, Alexus Devine, Heather Tillman, King Leung Fung, Wilfred D Vieira, Benjamin H Blehm, Yorihisa Kotobuki, Ben Busby, Emily I Chen, Kandice Tanner
BACKGROUND: Intrinsic and acquired resistance to drug therapies remains a challenge for malignant melanoma patients. Intratumoral heterogeneities within the tumor microenvironment contribute additional complexity to the determinants of drug efficacy and acquired resistance. METHODS: We use 3D biomimetic platforms to understand dynamics in extracellular matrix (ECM) biogenesis following pharmaceutical intervention against mitogen-activated protein kinases (MAPK) signaling...
March 5, 2016: BMC Cancer
Hala Kufaishi, May Alarab, Harold Drutz, Stephen Lye, Oksana Shynlova
BACKGROUND: This study tested a hypothesis that primary human vaginal cells derived from tissue of premenopausal women with severe pelvic organ prolapse (POP-HVCs) would display differential functional characteristics as compared to vaginal cells derived from asymptomatic women with normal pelvic floor support (control-HVCs). METHODS: Vaginal tissue biopsies were collected from premenopausal patients with POP (n = 8) and asymptomatic controls (n = 7) during vaginal hysterectomy or repair...
July 2016: Reproductive Sciences
Louise F Porter, Roberto Gallego-Pinazo, Catherine L Keeling, Martyna Kamieniorz, Nicoletta Zoppi, Marina Colombi, Cecilia Giunta, Richard Bonshek, Forbes D Manson, Graeme C Black
BACKGROUND: Brittle cornea syndrome (BCS) is a rare, generalized connective tissue disorder associated with extreme corneal thinning and a high risk of corneal rupture. Recessive mutations in transcription factors ZNF469 and PRDM5 cause BCS. Both transcription factors are suggested to act on a common pathway regulating extracellular matrix genes, particularly fibrillar collagens. We identified bilateral myopic choroidal neovascularization as the presenting feature of BCS in a 26-year-old-woman carrying a novel PRDM5 mutation (p...
November 11, 2015: Orphanet Journal of Rare Diseases
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