scholarly journals Endometrial Extracellular Matrix Rigidity and IFNτ to Ensure the Establishment of Early Pregnancy Through Activation of YAP

2020 ◽  
Author(s):  
Tao Zhang ◽  
Shuai Guo ◽  
Han Zhou ◽  
Zhimin Wu ◽  
Changwei Qiu ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Early Pregnancy ◽  
Matrix Rigidity

scholarly journals Endometrial extracellular matrix rigidity and IFNτ ensure the establishment of early pregnancy through activation of YAP

2021 ◽  
Author(s):  
Tao Zhang ◽  
Shuai Guo ◽  
Han Zhou ◽  
Zhimin Wu ◽  
Junfeng Liu ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Early Pregnancy ◽  
Matrix Rigidity

Extracellular Matrix Rigidity Modulates Human Cervical Smooth Muscle Contractility—New Insights into Premature Cervical Failure and Spontaneous Preterm Birth

2020 ◽  
Vol 28 (1) ◽  
pp. 237-251 ◽  
Author(s):  
Joy Vink ◽  
Victoria Yu ◽  
Sudip Dahal ◽  
James Lohner ◽  
Conrad Stern-Asher ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Preterm Birth ◽  
Matrix Rigidity ◽  
Spontaneous Preterm Birth ◽  
Muscle Contractility ◽  
Smooth Muscle Contractility

scholarly journals Expression of inter-alpha-trypsin inhibitor heavy chains in endometrium of cyclic and pregnant gilts

Reproduction ◽  
2003 ◽  
pp. 621-627 ◽  
Author(s):  
RD Geisert ◽  
MD Ashworth ◽  
Keyword(s):  
Gene Expression ◽  
Extracellular Matrix ◽  
Western Blot ◽  
Protease Inhibitor ◽  
Early Pregnancy ◽  
Trypsin Inhibitor ◽  
Serine Protease Inhibitor ◽  
Oestrous Cycle ◽  
Heavy Chains ◽  
Formation Of Complexes

Attachment of the placenta to the uterus in pigs involves extracellular interaction between the expanding trophoblastic membrane and the thick glycocalyx present on the uterine epithelial microvilli. Formation of complexes between members of inter-alpha-trypsin inhibitor family may function in the maintenance of the extracellular matrix. This study investigated the change in the inter-alpha-trypsin inhibitor heavy chains (ITIH1, ITIH2, ITIH3 and ITIH4) during the oestrous cycle and early pregnancy in pigs. Gene expression of ITIH1, ITIH2, ITIH3 and ITIH4 was detected in the endometrium of cyclic and pregnant gilts; however, gene expression of ITIH was not altered throughout the oestrous cycle or early pregnancy. Western blot analysis with an ITIH antiserum identified the possible linkage forms of ITIH with the serine protease inhibitor, bikunin. Pregnancy altered the release of the various inter-alpha-inhibitor forms from the endometrium during the period of trophoblastic attachment. The results from this study indicate that the inter-alpha-trypsin inhibitor family plays an important role in maintenance of the uterine surface glycocalyx during placental attachment in pigs.

scholarly journals Featured Article: TGF-β1 dominates extracellular matrix rigidity for inducing differentiation of human cardiac fibroblasts to myofibroblasts

2018 ◽  
Vol 243 (7) ◽  
pp. 601-612 ◽  
Author(s):  
Nathan Cho ◽  
Shadi E Razipour ◽  
Megan L McCain
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Cardiac Fibroblasts ◽  
Myofibroblast Differentiation ◽  
Matrix Rigidity ◽  
Growth Factor Beta ◽  
Human Cardiac Fibroblasts ◽  
Tgf Β1

Cardiac fibroblasts and their activated derivatives, myofibroblasts, play a critical role in wound healing after myocardial injury and often contribute to long-term pathological outcomes, such as excessive fibrosis. Thus, defining the microenvironmental factors that regulate the phenotype of cardiac fibroblasts and myofibroblasts could lead to new therapeutic strategies. Both chemical and biomechanical cues have previously been shown to induce myofibroblast differentiation in many organs and species. For example, transforming growth factor beta 1, a cytokine secreted by neutrophils, and rigid extracellular matrix environments have both been shown to promote differentiation. However, the relative contributions of transforming growth factor beta 1 and extracellular matrix rigidity, two hallmark cues in many pathological myocardial microenvironments, to the phenotype of human cardiac fibroblasts are unclear. We hypothesized that transforming growth factor beta 1 and rigid extracellular matrix environments would potentially have a synergistic effect on the differentiation of human cardiac fibroblasts to myofibroblasts. To test this, we seeded primary human adult cardiac fibroblasts onto coverslips coated with polydimethylsiloxane of various elastic moduli, introduced transforming growth factor beta 1, and longitudinally quantified cell phenotype by measuring expression of α-smooth muscle actin, the most robust indicator of myofibroblasts. Our data indicate that, although extracellular matrix rigidity influenced differentiation after one day of transforming growth factor beta 1 treatment, ultimately transforming growth factor beta 1 superseded extracellular matrix rigidity as the primary regulator of myofibroblast differentiation. We also measured expression of POSTN, FAP, and FSP1, proposed secondary indicators of fibroblast/myofibroblast phenotypes. Although these genes partially trended with α-smooth muscle actin expression, they were relatively inconsistent. Finally, we demonstrated that activated myofibroblasts incompletely revert to a fibroblast phenotype after they are re-plated onto new surfaces without transforming growth factor beta 1, suggesting differentiation is partially reversible. Our results provide new insights into how microenvironmental cues affect human cardiac fibroblast differentiation in the context of myocardial pathology, which is important for identifying effective therapeutic targets and dictating supporting cell phenotypes for engineered human cardiac disease models. Impact statement Heart disease is the leading cause of death worldwide. Many forms of heart disease are associated with fibrosis, which increases extracellular matrix (ECM) rigidity and compromises cardiac output. Fibrotic tissue is synthesized primarily by myofibroblasts differentiated from fibroblasts. Thus, defining the cues that regulate myofibroblast differentiation is important for understanding the mechanisms of fibrosis. However, previous studies have focused on non-human cardiac fibroblasts and have not tested combinations of chemical and mechanical cues. We tested the effects of TGF-β1, a cytokine secreted by immune cells after injury, and ECM rigidity on the differentiation of human cardiac fibroblasts to myofibroblasts. Our results indicate that differentiation is initially influenced by ECM rigidity, but is ultimately superseded by TGF-β1. This suggests that targeting TGF-β signaling pathways in cardiac fibroblasts may have therapeutic potential for attenuating fibrosis, even in rigid microenvironments. Additionally, our approach can be leveraged to engineer more precise multi-cellular human cardiac tissue models.

scholarly journals Linking Extracellular Matrix Agrin to the Hippo Pathway in Liver Cancer and Beyond

Cancers ◽  
2018 ◽  
Vol 10 (2) ◽  
pp. 45 ◽  
Author(s):  
Sayan Chakraborty ◽  
Wanjin Hong
Keyword(s):  
Extracellular Matrix ◽  
Neuromuscular Junctions ◽  
Hippo Pathway ◽  
Cardiac Regeneration ◽  
Matrix Rigidity ◽  
Macroscopic Scale ◽  
Cellular Processes ◽  
Scale Matrix ◽  
The Hippo Pathway

In addition to the structural and scaffolding role, the extracellular matrix (ECM) is emerging as a hub for biomechanical signal transduction that is frequently relayed to intracellular sensors to regulate diverse cellular processes. At a macroscopic scale, matrix rigidity confers long-ranging effects contributing towards tissue fibrosis and cancer. The transcriptional co-activators YAP/TAZ, better known as the converging effectors of the Hippo pathway, are widely recognized for their new role as nuclear mechanosensors during organ homeostasis and cancer. Still, how YAP/TAZ senses these “stiffness cues” from the ECM remains enigmatic. Here, we highlight the recent perspectives on the role of agrin in mechanosignaling from the ECM via antagonizing the Hippo pathway to activate YAP/TAZ in the contexts of cancer, neuromuscular junctions, and cardiac regeneration.

Tenascin is induced at implantation sites in the mouse uterus and interferes with epithelial cell adhesion

Development ◽  
1994 ◽  
Vol 120 (3) ◽  
pp. 661-671 ◽  
Author(s):  
J. Julian ◽  
R. Chiquet-Ehrismann ◽  
H.P. Erickson ◽  
D.D. Carson
Keyword(s):  
Extracellular Matrix ◽  
Cell Adhesion ◽  
Epithelial Cell ◽  
Early Pregnancy ◽  
Matrix Protein ◽  
Cellular Adhesion ◽  
Uterine Epithelium ◽  
Extracellular Matrix Protein ◽  
Mouse Uterus ◽  
Uterine Epithelial Cell

Expression of tenascin, an extracellular matrix protein associated with morphogenetic events and altered states of cellular adhesion, was examined in mouse uterus during the peri-implantation period. A uniform low level expression of tenascin was detected in stromal extracellular matrix during the estrous cycle and days 1 through 4 of early pregnancy. During the period of blastocyst attachment (day 4.5), an intense deposition of tenascin fibrils was located in the extracellular matrix of stroma immediately subjacent to the uterine epithelium surrounding the attaching blastocyst. This localized intensity of tenascin expression was both spatially and temporally restricted. By day 5.5, differentiation of stroma in the immediate area around the embryo to form the primary decidual zone was accompanied by a reduced amount of tenascin expression in the form of fragmented fibrils. Tenascin also could be induced by an artificial stimulus in uterine stroma of mice that had been hormonally prepared for implantation. The ability of artificial stimuli to induce tenascin expression suggested that the tenascin-inducing signals were derived from uterine cells, presumably lumenal epithelium, rather than embryonic cells. Consistent with this, conditioned medium from primary cultures of uterine epithelium was found to induce tenascin expression (2- to 4-fold) in isolated uterine stroma. Artificial stimuli generated a temporal pattern of tenascin expression similar to that observed during early pregnancy; however, in the artificially induced model, tenascin was induced in stroma immediately subjacent to lumenal epithelium along the entire length of the uterus. Purified tenascin and a recombinant tenascin fragment consisting of alternatively spliced fibronectin type III repeats, interfered with maintenance of uterine epithelial cell adhesion to Matrigel. In contrast, other recombinant tenascin fragments or fibronectin had no effect in this regard. Tenascin had no effect on adhesion of uterine stroma. Collectively, these results suggest that stimulation of TN expression in stromal extracellular matrix in vivo occurs via hormonally regulated, epithelial-mesenchymal interactions and serves as an early marker for uterine receptivity and the attachment phase of implantation. Furthermore, tenascin may facilitate embryo penetration by disrupting uterine epithelial cell adhesion to underlying basal lamina.

Extracellular matrix rigidity governs smooth muscle cell motility in a biphasic fashion

2005 ◽  
Vol 204 (1) ◽  
pp. 198-209 ◽  
Author(s):  
Shelly R. Peyton ◽  
Andrew J. Putnam
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Cell Motility ◽  
Muscle Cell ◽  
Matrix Rigidity
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