Regulation of α-Smooth Muscle Actin Protein Expression in Adipose-Derived Stem Cells

2006 ◽  
Vol 183 (2) ◽  
pp. 80-86 ◽  
Author(s):  
Wen-Chi C. Lee ◽  
J. Peter Rubin ◽  
Kacey G. Marra
Keyword(s):  
Stem Cells ◽  
Smooth Muscle ◽  
Protein Expression ◽  
Smooth Muscle Actin ◽  
Adipose Derived Stem Cells ◽  
Muscle Actin ◽  
Actin Protein

scholarly journals Concerted Upregulation of CLP36 and Smooth Muscle Actin Protein Expression in Human Endometrium during Decidualization

2005 ◽  
Vol 179 (3) ◽  
pp. 109-114 ◽  
Author(s):  
Ulrich Miehe ◽  
Peruka Neumaier-Wagner ◽  
Mamed Kadyrov ◽  
Pankaj Goyal ◽  
Joachim Alfer ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Expression ◽  
Smooth Muscle Actin ◽  
Human Endometrium ◽  
Muscle Actin ◽  
Actin Protein

Regulation of airway smooth muscle α-actin expression by glucocorticoids

2007 ◽  
Vol 292 (1) ◽  
pp. L99-L106 ◽  
Author(s):  
Adam M. Goldsmith ◽  
Marc B. Hershenson ◽  
Miguel P. Wolbert ◽  
J. Kelley Bentley
Keyword(s):  
Smooth Muscle ◽  
Protein Expression ◽  
Airway Smooth Muscle ◽  
Contractile Function ◽  
Smooth Muscle Actin ◽  
Mrna Translation ◽  
Contractile Protein ◽  
Muscle Actin ◽  
Actin Expression ◽  
Actin Protein

Airway smooth muscle hypertrophy appears to be present in severe asthma. However, the effect of corticosteroids on airway smooth muscle cell size or contractile protein expression has not been studied. We examined the effects of dexamethasone, fluticasone, and salmeterol on contractile protein expression in transforming growth factor (TGF)-β-treated primary bronchial smooth muscle cells. Dexamethasone and fluticasone, but not salmeterol, each reduced expression of α-smooth muscle actin and the short isoform of myosin light chain kinase. Steady-state α-actin mRNA level and stability were unchanged, consistent with posttranscriptional control. Fluticasone significantly decreased α-actin protein synthesis following treatment with the transcriptional inhibitor actinomycin D, indicative of an inhibitory effect on mRNA translation. Fluticasone also significantly increased α-actin protein turnover. Finally, fluticasone reduced TGF-β-induced incorporation of α-actin into filamentous actin, cell length, and cell shortening in response to ACh and KCl. We conclude that glucocorticoids reduce human airway smooth muscle α-smooth muscle actin expression and incorporation into contractile filaments, as well as contractile function, in part by attenuation of mRNA translation and enhancement of protein degradation.

scholarly journals Mesenchymal Stem Cells From Adipose Tissue Do not Improve Functional Recovery After Ischemic Stroke in Hypertensive Rats

Stroke ◽  
2020 ◽  
Vol 51 (1) ◽  
pp. 342-346 ◽  
Author(s):  
Luke Diekhorst ◽  
Mari Carmen Gómez-de Frutos ◽  
Fernando Laso-García ◽  
Laura Otero-Ortega ◽  
Blanca Fuentes ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Adipose Tissue ◽  
Smooth Muscle ◽  
Ischemic Stroke ◽  
Smooth Muscle Actin ◽  
Lesion Size ◽  
Muscle Actin ◽  
Hypertensive Rats ◽  
Vascular Markers

Background and Purpose— Hypertension is the most frequent comorbidity in stroke.The purpose of this study was to evaluate whether hypertension alters the response to treatment with adipose tissue-derived mesenchymal stem cells (ADMSCs) after an ischemic stroke in rats. Methods— Ischemic stroke was induced in male normotensive or hypertensive rats. Either vehicle or 1×10 6 ADMSC was intravenously administered at 48 hours poststroke. Functional outcome, lesion size and volume, and markers of brain repair (GFAP [glial fibrillary acidic protein], doublecortin, CD-31, α-smooth muscle actin) were evaluated. Results— Hypertensive rats had larger lesions, higher apparent diffusion coefficients (ADC) and worse functional outcomes than normotensive rats. Hypertension increased GFAP and vascular markers (CD-31 and α-smooth muscle actin). The hypertensive rats treated with ADMSC did not show any significant improvement in functional recovery, lesion size, ADC values, or histological markers compared with those which received the vehicle. Conclusions— ADMSC did not reverse the hypertension-induced increase in lesion severity or functional impairment. Gliosis, neurogenesis, or vascular markers were not affected by ADMSC in hypertensive rats. Hypertension has a negative impact on the therapeutic effect of ADMSC after an ischemic stroke.

scholarly journals Isolation and Functional Characterization of α-Smooth Muscle Actin Expressing Cardiomyocytes from Embryonic Stem Cells

2010 ◽  
Vol 25 (6) ◽  
pp. 595-604 ◽  
Author(s):  
Shiva Prasad Potta ◽  
Huamin Liang ◽  
Johannes Winkler ◽  
Michael Xavier Doss ◽  
Shuhua Chen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Smooth Muscle ◽  
Embryonic Stem Cells ◽  
Smooth Muscle Actin ◽  
Functional Characterization ◽  
Embryonic Stem ◽  
Muscle Actin

Alpha-smooth muscle actin expression and structure integrity in chondrogenesis of human mesenchymal stem cells

2006 ◽  
Vol 324 (3) ◽  
pp. 457-466 ◽  
Author(s):  
Shih-Chieh Hung ◽  
Pei-Yin Kuo ◽  
Ching-Fang Chang ◽  
Tain-Hsiung Chen ◽  
Larry Low-Tone Ho
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Human Mesenchymal Stem Cells ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Actin Expression

scholarly journals Human adipose-derived mesenchymal stem cells accelerate decellularized neobladder regeneration

2019 ◽  
Vol 7 (2) ◽  
pp. 161-169 ◽  
Author(s):  
Victoria Moreno-Manzano ◽  
Maravillas Mellado-López ◽  
Maria Jose Morera-Esteve ◽  
Ana Alastrue-Agudo ◽  
Viviana Bisbal-Velasco ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bladder Cancer ◽  
Mesenchymal Stem Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Submucosal Layer ◽  
Muscle Actin ◽  
Cytokeratin 7 ◽  
Longitudinal Smooth Muscle ◽  
Bladder Substitution

Abstract Decellularized natural bladder matrices (neobladders) represent an exciting means to regenerate the bladder following bladder cancer-associated cystectomy. In this study, we compare the evolution of decellularized matrices with recellularized matrices by seeding it with human adipose-derived mesenchymal stem cells (ADSC) after implantation following partial cystectomy in rats. We discovered significant anatomical differences since 10 days after neobladder implantation with the ADSC-containing matrices promoting a significant recovery of mature p63- and cytokeratin 7-positive urothelium. We also discovered significantly induced expression of the vimentin mesoderm marker in the submucosal layer in ADSC-seeded matrices. Interestingly, we found a higher expression of smooth muscle actin in transversal and longitudinal smooth muscle layers with ADSC-seeded matrices. Furthermore, ADSC also showed increased vascularization and nerve innervation of the neobladder as determined by the distribution of CD31 and S100β reactivity, respectively. We believe that ADSC and their paracrine-acting pro-regenerative secretome within decellularized matrices represent an efficient bladder substitution strategy; however, we require a fuller understanding of the mechanisms involved before clinical studies can begin.

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