scholarly journals Heparin Mimicking Polymer Promotes Myogenic Differentiation of Muscle Progenitor Cells

2010 ◽  
Vol 11 (12) ◽  
pp. 3294-3300 ◽  
Author(s):  
Nivedita Sangaj ◽  
Phillip Kyriakakis ◽  
Darren Yang ◽  
Chien-Wen Chang ◽  
Gaurav Arya ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Myogenic Differentiation ◽  
Muscle Progenitor Cells

The homeobox gene Msx1 is expressed in a subset of somites, and in muscle progenitor cells migrating into the forelimb

Development ◽  
1999 ◽  
Vol 126 (12) ◽  
pp. 2689-2701 ◽  
Author(s):  
D. Houzelstein ◽  
G. Auda-Boucher ◽  
Y. Cheraud ◽  
T. Rouaud ◽  
I. Blanc ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Myogenic Differentiation ◽  
Homeobox Gene ◽  
Limb Bud ◽  
Axial Position ◽  
Limb Muscle ◽  
Pax3 Gene ◽  
Muscle Progenitor Cells ◽  
Myoblast Cell

In myoblast cell cultures, the Msx1 protein is able to repress myogenesis and maintain cells in an undifferentiated and proliferative state. However, there has been no evidence that Msx1 is expressed in muscle or its precursors in vivo. Using mice with the nlacZ gene integrated into the Msx1 locus, we show that the reporter gene is expressed in the lateral dermomyotome of brachial and thoracic somites. Cells from this region will subsequently contribute to forelimb and intercostal muscles. Using Pax3 gene transcripts as a marker of limb muscle progenitor cells as they migrate from the somites, we have defined precisely the somitic origin and timing of cell migration from somites to limb buds in the mouse. Differences in the timing of migration between chick and mouse are discussed. Somites that label for Msx1(nlacZ)transgene expression in the forelimb region partially overlap with those that contribute Pax3-expressing cells to the forelimb. In order to see whether Msx1 is expressed in this migrating population, we have grafted somites from the forelimb level of Msx1(nlacZ)mouse embryos into a chick host embryo. We show that most cells migrating into the wing field express the Msx1(nlacZ)transgene, together with Pax3. In these experiments, Msx1 expression in the somite depends on the axial position of the graft. Wing mesenchyme is capable of inducing Msx1 transcription in somites that normally would not express the gene; chick hindlimb mesenchyme, while permissive for this expression, does not induce it. In the mouse limb bud, the Msx1(nlacZ)transgene is downregulated prior to the activation of the Myf5 gene, an early marker of myogenic differentiation. These observations are consistent with the proposal that Msx1 is involved in the repression of muscle differentiation in the lateral half of the somite and in limb muscle progenitor cells during their migration.

scholarly journals Smooth Muscle Progenitor Cells: Friend or Foe in Vascular Disease?

2009 ◽  
Vol 4 (2) ◽  
pp. 131-140 ◽  
Author(s):  
Olivia Oostrom ◽  
Joost Fledderus ◽  
Dominique de Kleijn ◽  
Gerard Pasterkamp ◽  
Marianne Verhaar
Keyword(s):  
Smooth Muscle ◽  
Vascular Disease ◽  
Progenitor Cells ◽  
Muscle Progenitor Cells

Advanced maturation by electrical stimulation: Differences in response between C2C12 and primary muscle progenitor cells

2010 ◽  
Vol 5 (7) ◽  
pp. 529-539 ◽  
Author(s):  
Marloes L. P. Langelaan ◽  
Kristel J. M. Boonen ◽  
Kang Yuen Rosaria-Chak ◽  
Daisy W. J. van der Schaft ◽  
Mark J. Post ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Progenitor Cells ◽  
Muscle Progenitor Cells

Abstract 1451: Hyperpolarization Induces Differentiation Of Human Cardiomyocyte Progenitor Cells

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Piet van Vliet ◽  
Teun P de Boer ◽  
Marcel A van der Heyden ◽  
Joost P Sluijter ◽  
Pieter A Doevendans ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Molecular Mechanisms ◽  
Troponin I ◽  
Lucifer Yellow ◽  
Myogenic Differentiation ◽  
Luciferase Reporter ◽  
Dependent Manner ◽  
Cardiomyogenic Differentiation ◽  
Low Potassium ◽  
Calcineurin Signaling

Background: Recently, we have isolated cardiomyocyte progenitor cells (hCMPCs) from human fetal and adult hearts. These cells differentiate into spontaneously beating cardiomyocytes when stimulated with 5-azacytidine. Subsequent stimulation by TGFβ enhances differentiation efficiency to nearly 100%. The underlying molecular mechanisms mediating this cardiomyogenic differentiation are not understood. In skeletal myoblasts, hyperpolarization-mediated activation of calcineurin signaling is crucial for myogenic differentiation. In hCMPCs, whole-cell patch clamp recordings showed a hyperpolarized membrane potential after stimulation with TGFβ or BMP. We hypothesized that hyperpolarization and calcineurin signaling regulate cardiomyogenic differentiation of hCMPCs after TGFβ stimulation. Methods & Results: To test whether hyperpolarization initiates cardiomyogenic differentiation, hyperpolarization was induced by 1) co-culture of hCMPCs with HEK 293 cells overexpressing a Kir2.1GFP fusion protein (KWGF cells) or 2) culture of hCMPCs overnight in medium containing low potassium concentrations. During co-culture, Lucifer Yellow dye injection in KWGF cells spread to neighboring hCMPCs, indicating cellular coupling. This resulted in stable hyperpolarization in hCMPCs, which could be blocked by addition of the gap junction inhibitor halothane. After two weeks, qPCR analysis revealed increased expression of cardiac sarcomeric genes in the hCMPCs in a dose-dependent manner. Induction of hyperpolarization by culturing hCMPCs with low potassium concentrations also resulted in increased expression of cardiac genes and the formation of spontaneously beating cells. Immunofluorescence staining revealed striated patterns of troponin I and α-actinin. Interestingly, hyperpolarization also increased intracellular calcium levels in hCMPCs, as measured by ratiometric imaging of indo-1 fluorescence, and, subsequently, a time-dependent increase in NFAT-Luciferase reporter activity, indicating activation of the calcineurin pathway. Conclusion: TGFβ and/or BMP-mediated hyperpolarization of hCMPCs induces calcineurin-mediated cardiomyogenic differentiation.

scholarly journals Syndecan-4-Expressing Muscle Progenitor Cells in the SP Engraft as Satellite Cells during Muscle Regeneration

2009 ◽  
Vol 4 (3) ◽  
pp. 217-225 ◽  
Author(s):  
Kathleen Kelly Tanaka ◽  
John K. Hall ◽  
Andrew A. Troy ◽  
D.D.W. Cornelison ◽  
Susan M. Majka ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Satellite Cells ◽  
Muscle Regeneration ◽  
Muscle Progenitor Cells

scholarly journals Reduction of Connexin 43 Attenuates Angiogenic Effects of Human Smooth Muscle Progenitor Cells via Inactivation of Akt and NF-κB Pathway

2020 ◽  
Author(s):  
Ting-Yi Tien ◽  
Yih-Jer Wu ◽  
Cheng-Huang Su ◽  
Hsueh-Hsiao Wang ◽  
Chin-Ling Hsieh ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Progenitor Cells ◽  
Connexin 43 ◽  
Paracrine Effects ◽  
Angiogenic Potential ◽  
Junction Protein ◽  
Src Activation ◽  
Muscle Progenitor Cells

Objective: Circulating progenitor cells possess vasculogenesis property and participate in repair of vascular injury. Cx (connexin) 43—a transmembrane protein constituting gap junctions—is involved in vascular pathology. However, the role of Cx43 in smooth muscle progenitor cells (SPCs) remained unclear. Approach and Results: Human SPCs cultured from CD34 + peripheral blood mononuclear cells expressed smooth muscle cell markers, such as smooth muscle MHC (myosin heavy chain), nonmuscle MHC, calponin, and CD140B, and Cx43 was the most abundant Cx isoform. To evaluate the role of Cx43 in SPCs, short interference RNA was used to knock down Cx43 expression. Cellular activities of SPCs were reduced by Cx43 downregulation. In addition, Cx43 downregulation attenuated angiogenic potential of SPCs in hind limb ischemia mice. Protein array and ELISA of the supernatant from SPCs showed that IL (interleukin)-6, IL-8, and HGF (hepatocyte growth factor) were reduced by Cx43 downregulation. Simultaneously, Cx43 downregulation reduced the phosphorylation of NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) and Akt (protein kinase B) pathway and reactivation of NF-κB and Akt using betulinic acid, and SC79 could restore the secretion of growth factors and cytokines. Moreover, FAK (focal adhesion kinase)-Src (proto-oncogene tyrosine-protein kinase Src) activation was increased by Cx43 downregulation, and inactivation of Akt–NF-κB could be restored by Src inhibitor (PP2), indicating that Akt–NF-κB inactivated by Cx43 downregulation arose from FAK-Src activation. Finally, the depressed cellular activities and secretion of SPCs after Cx43 downregulation were restored by FAK inhibitor PF-562271 or PP2. Conclusions: SPCs possess angiogenic potential to repair ischemic tissue mainly through paracrine effects. Gap junction protein Cx43 plays an important role in regulating cellular function and paracrine effects of SPCs through FAK-Src axis.

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