Attenuation of Expression of Splenocytes Pro-Inflammatory Cytokines and Lung Alpha-Smooth Muscle Actin By Human Amniotic Mesenchymal Stem Cells-Conditioned Medium in Asthmatic Mice

2021 ◽  
Author(s):  
Fereshteh Dalouchi ◽  
Zeynab Sharifi Aghdam ◽  
Raza Falak ◽  
Morteza Bakhshesh ◽  
Maryam Hajidazeh ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Smooth Muscle ◽  
Inflammatory Cytokines ◽  
Smooth Muscle Actin ◽  
Inflammatory Factors ◽  
Muscle Actin ◽  
Alpha Smooth Muscle Actin ◽  
Amniotic Mesenchymal Stem Cells ◽  
Pro Inflammatory Cytokines

Abstract Background Asthma is a chronic respiratory illness characterized by lung tissue remodeling, T helper cell imbalance, and the generation of inflammatory factors. The Human amniotic mesenchymal stem cells-conditioned medium (hAM-MSC-CM) contains various immunomodulatory components and has been utilized in certain studies as a source for anti-inflammatory factors. We investigated the impacts of CM on splenocytes pro-inflammatory cytokines and alpha-smooth muscle actin (α-SMA) expression in Balb/c mice with Ovalbumin (OVA)-induced asthma.Methods and results Forty mice were separated into four groups of ten: control (challenged and sensitized with normal saline solution), asthma (sensitized on days 1, 8, and 14 and challenged daily with OVA from days 21 to 28), OVA+CM (asthmatic mice treated with CM on days 29 and 30), and OVA+DMEM (DMEM-treated asthmatic mice on days 29 and 30). The spleen and lung tissues were removed 48 hours after the final challenge, and the expression of the inflammatory factors in the splenocyte culture supernatant was determined by ELISA, while the α-SMA expression in the lung was determined using western blotting. α-SMA protein expression was significantly greater in lung tissue. Also, inflammatory agents were significantly higher in the splenocytes supernatant in the DMEM and asthma groups compared to the control group. CM therapy has been shown to inhibit the production of the α-SMA protein and inflammatory cytokines. Conclusions Results showed that CM Treatment was able to decrease the α-SMA expression in lung and splenocytes pro-inflammatory cytokines.

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 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 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.

scholarly journals Multiple Myeloma-Derived Exosomes Regulate the Functions of Mesenchymal Stem Cells Partially via Modulating miR-21 and miR-146a

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Qian Cheng ◽  
Xin Li ◽  
Jingru Liu ◽  
Qinmao Ye ◽  
Yanfang Chen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Multiple Myeloma ◽  
Mesenchymal Stem Cells ◽  
Smooth Muscle ◽  
Cancer Cells ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Cancer Associated Fibroblast ◽  
Secretion Inhibition

Exosomes derived from cancer cells can affect various functions of mesenchymal stem cells (MSCs) via conveying microRNAs (miRs). miR-21 and miR-146a have been demonstrated to regulate MSC proliferation and transformation. Interleukin-6 (IL-6) secreted from transformed MSCs in turn favors the survival of multiple myeloma (MM) cells. However, the effects of MM exosomes on MSC functions remain largely unclear. In this study, we investigated the effects of OPM2 (a MM cell line) exosomes (OPM2-exo) on regulating the proliferation, cancer-associated fibroblast (CAF) transformation, and IL-6 secretion of MSCs and determined the role of miR-21 and miR-146a in these effects. We found that OPM2-exo harbored high levels of miR-21 and miR-146a and that OPM2-exo coculture significantly increased MSC proliferation with upregulation of miR-21 and miR-146a. Moreover, OPM2-exo induced CAF transformation of MSCs, which was evidenced by increased fibroblast-activated protein (FAP), α-smooth muscle actin (α-SMA), and stromal-derived factor 1 (SDF-1) expressions and IL-6 secretion. Inhibition of miR-21 or miR-146a reduced these effects of OPM2-exo on MSCs. In conclusion, MM could promote the proliferation, CAF transformation, and IL-6 secretion of MSCs partially through regulating miR21 and miR146a.

scholarly journals Umbilical cord/placenta-derived mesenchymal stem cells inhibit fibrogenic activation in human intestinal myofibroblasts via inhibition of myocardin-related transcription factor A

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Yoon Jeong Choi ◽  
Jun Bon Koo ◽  
Hee Yeon Kim ◽  
Jin Won Seo ◽  
Eun Jeong Lee ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Transcription Factor ◽  
Smooth Muscle ◽  
Umbilical Cord ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Intestinal Fibrosis ◽  
Related Transcription Factor ◽  
Tgf Β1

Abstract Background The lack of anti-fibrotic agents targeting intestinal fibrosis is a large unmet need in inflammatory bowel diseases, including Crohn’s disease and ulcerative colitis. Previous studies have found that perinatal tissue (umbilical cord, UC; placenta, PL)-derived mesenchymal stem cells (MSCs) reduce fibrosis in several organs. However, their effects on human intestinal fibrosis are poorly understood. This study investigated the anti-fibrogenic properties and mechanisms of MSCs derived from UC and PL (UC/PL-MSCs) on human primary intestinal myofibroblasts (HIMFs). Methods The HIMFs were treated with TGF-β1 and co-cultured with UC/PL-MSCs. We used a small molecular inhibitor CCG-100602 to examine whether serum response factor (SRF) and its transcriptional cofactor myocardin-related transcription factor A (MRTF-A) are involved in TGF-β1-induced fibrogenic activation in HIMFs. The anti-fibrogenic mechanism of UC/PL-MSCs on HIMFs was analyzed by detecting the expression of RhoA, MRTF-A, and SRF in HIMFs. Results UC/PL-MSCs reduced TGF-β1-induced procollagen1A1, fibronectin, and α-smooth muscle actin expression in HIMFs. This anti-fibrogenic effect was more apparent in the UC-MSCs. TGF-β1 stimulation increased the expressions of RhoA, MRTF-A, and SRF in the HIMFs. TGF-β1 induced the synthesis of procollagen1A1, fibronectin, and α-smooth muscle actin through a MRTF-A/SRF-dependent mechanism. Co-culture with the UC/PL-MSCs downregulated fibrogenesis by inhibition of RhoA, MRTF-A, and SRF expression. Conclusions UC/PL-MSCs suppress TGF-β1-induced fibrogenic activation in HIMFs by blocking the Rho/MRTF/SRF pathway and could be considered as a novel candidate for stem cell-based therapy of intestinal fibrosis.

scholarly journals Hypoxia Mesenchymal Stem Cells Accelerate Wound Closure Improvement by Controlling α-smooth Muscle actin Expression in the Full-thickness Animal Model

2021 ◽  
Vol 9 (A) ◽  
pp. 35-41
Author(s):  
Nur Fitriani Hamra ◽  
Agung Putra ◽  
Arya Tjipta ◽  
Nur Dina Amalina ◽  
Taufiqurrachman Nasihun
Keyword(s):  
Stem Cells ◽  
Wound Healing ◽  
Mesenchymal Stem Cells ◽  
Smooth Muscle ◽  
Wound Closure ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Full Thickness ◽  
Treatment Groups ◽  
All Treatment

BACKGROUND: The active myofibroblast producing extracellular matrix deposition regarding wound closure is characterized by alpha-smooth muscle actin (α-SMA) expression. However, the persistence of α-SMA expression due to prolonged inflammation may trigger scar formation. A new strategy to control α-SMA expression in line with wound closure improvement uses hypoxic mesenchymal stem cells (HMSCs) due to their ability to firmly control inflammation for early initiating cell proliferation, including the regulation of α-SMA expression associated with wound closure acceleration. AIM: This study aimed to explore the role of HMSCs in accelerating the optimum wound closure percentages through controlling the α-SMA expression. MATERIALS AND METHODS: Twenty-four full-thickness rats wound model were randomly divided into four groups: Sham (Sh), Control (C) by NaCl administration only, and two treatment groups by HMSCs at doses of 1.5×106 cells (T1) and HMSCs at doses of 3×106 cells (T2). HMSCs were incubated under hypoxic conditions. The α-SMA expression was analyzed under immunohistochemistry staining assay, and the wound closure percentage was analyzed by ImageJ software. RESULTS: This study showed a significant increase in wound closure percentage in all treatment groups that gradually initiated on days 6 and 9 (p < 0.05). In line with the increase of wound closure percentages on day 9, there was also a significant decrease in α-SMA expression in all treatment groups (p < 0.05), indicating the optimum wound healing has preceded. CONCLUSION: HMSCs have a robust ability to accelerated wound closure improvement to the optimum wound healing by controlling α-SMA expression depending on wound healing phases.

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