Effects of growth rate and cell density on nerve growth factor secretion in cultures of vascular and bladder smooth muscle cells from hypertensive and hyperactive rats

1998 ◽  
Vol 294 (3) ◽  
pp. 431-438 ◽  
Author(s):  
David B. Clemow ◽  
J. B. Tuttle
Keyword(s):  
Growth Rate ◽  
Smooth Muscle ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Cell Density ◽  
Muscle Cells ◽  
Bladder Smooth Muscle ◽  
Factor Secretion ◽  
Growth Factor Secretion

Thrombin regulates nerve growth factor secretion from vascular, but not bladder smooth muscle cells

1997 ◽  
Vol 289 (1) ◽  
pp. 155-161 ◽  
Author(s):  
T. B. Sherer ◽  
J. M. Spitsbergen ◽  
W. D. Steers ◽  
J. B. Tuttle
Keyword(s):  
Smooth Muscle ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Bladder Smooth Muscle ◽  
Nerve Growth ◽  
Factor Secretion ◽  
Growth Factor Secretion

scholarly journals Human iPSC-Derived Vascular Smooth Muscle Cells in a Fibronectin Functionalized Collagen Hydrogel Augment Endothelial Cell Morphogenesis

2021 ◽  
Vol 8 (12) ◽  
pp. 223
Author(s):  
Kaiti Duan ◽  
Biraja C. Dash ◽  
Daniel C. Sasson ◽  
Sara Islam ◽  
Jackson Parker ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Mechanistic Study ◽  
Αvβ3 Integrin ◽  
Factor Secretion ◽  
Growth Factor Secretion

Tissue-engineered constructs have immense potential as autologous grafts for wound healing. Despite the rapid advancement in fabrication technology, the major limitation is controlling angiogenesis within these constructs to form a vascular network. Here, we aimed to develop a 3D hydrogel that can regulate angiogenesis. We tested the effect of fibronectin and vascular smooth muscle cells derived from human induced pluripotent stem cells (hiPSC-VSMC) on the morphogenesis of endothelial cells. The results demonstrate that fibronectin increases the number of EC networks. However, hiPSC-VSMC in the hydrogel further substantiated the number and size of EC networks by vascular endothelial growth factor and basic fibroblast growth factor secretion. A mechanistic study shows that blocking αvβ3 integrin signaling between hiPSC-VSMC and fibronectin impacts the EC network formation via reduced cell viability and proangiogenic growth factor secretion. Collectively, this study set forth initial design criteria in developing an improved pre-vascularized construct.

The production of nerve growth factor by human bladder smooth muscle cells in vivo and in vitro

2000 ◽  
Vol 85 (9) ◽  
pp. 1115-1119 ◽  
Author(s):  
R. Tanner ◽  
P. Chambers ◽  
M.H. Khadra ◽  
J.I. Gillespie
Keyword(s):  
Smooth Muscle ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Bladder Smooth Muscle ◽  
Human Bladder ◽  
Nerve Growth

Cyclic stretch activates p38 SAPK2-, ErbB2-, and AT1-dependent signaling in bladder smooth muscle cells

2000 ◽  
Vol 279 (4) ◽  
pp. C1155-C1167 ◽  
Author(s):  
Hiep T. Nguyen ◽  
Rosalyn M. Adam ◽  
Samuel H. Bride ◽  
John M. Park ◽  
Craig A. Peters ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Mapk Pathway ◽  
Muscle Cells ◽  
Cyclic Stretch ◽  
Bladder Smooth Muscle ◽  
Erk Mapk

Cyclic mechanical stretch of bladder smooth muscle cells (SMC) increases rates of DNA synthesis and stimulates transcription of the gene for heparin-binding epidermal growth factor-like growth factor (HB-EGF), an ErbB1/EGF receptor ligand that has been linked to hypertrophic bladder growth. In this study we sought to clarify the signaling pathways responsible for mechanotransduction of the stretch stimulus. HB-EGF mRNA levels, DNA synthesis, and AP-1/Ets DNA binding activities were induced by repetitive stretch of primary culture rat bladder SMC. Inhibitors of the p38 SAPK2 pathway, the angiotensin receptor type 1 (AT1), and the ErbB2 tyrosine kinase reduced each of these activities, while an inhibitor of the extracellular signal-regulated kinase mitogen-activated protein kinase (Erk-MAPK) pathway had no effect. Stretch rapidly activated stress-activated protein kinase 2 (p38 SAPK2) and Jun NH2-terminal kinase (JNK)/SAPK pathways but not the Erk-MAPK pathway and induced ErbB2 but not ErbB1 phosphorylation. Angiotensin II (ANG II) a bladder SMC mitogen previously linked to the stretch response, did not activate ErbB2, and ErbB2 activation occurred in response to stretch in the presence of an ANG receptor inhibitor, indicating that activation of the AT1-mediated pathway and the ErbB2-dependent pathway occurs by independent mechanisms. p38 SAPK2 and JNK/SAPK signaling also appeared to be independent of the ErbB2 and AT1 pathways. These findings indicate that stretch-stimulated DNA synthesis and gene expression in normal bladder SMC occur via multiple independent receptor systems (e.g., AT1 and ErbB2) and at least one MAPK pathway (p38 SAPK2). Further, we show that the Erk-MAPK pathway, which in most systems is linked to receptor-dependent cell growth responses, is not involved in progression to DNA synthesis or in the response of the HB-EGF gene to mechanical forces.

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