scholarly journals Evidence for Vitamin D Receptor Expression and Direct Effects of 1α,25(OH)2D3 in Human Skeletal Muscle Precursor Cells

Endocrinology ◽  
2016 ◽  
Vol 157 (1) ◽  
pp. 98-111 ◽  
Author(s):  
Karl Olsson ◽  
Amarjit Saini ◽  
Anna Strömberg ◽  
Seher Alam ◽  
Mats Lilja ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Vitamin D Receptor ◽  
Human Skeletal Muscle ◽  
Precursor Cells ◽  
Receptor Expression ◽  
Direct Effects ◽  
Muscle Precursor ◽  
Muscle Precursor Cells

scholarly journals Enhanced proliferation of human skeletal muscle precursor cells derived from elderly donors cultured in estimated physiological (5%) oxygen

2009 ◽  
Vol 61 (3) ◽  
pp. 93-107 ◽  
Author(s):  
Sheree D. Martin ◽  
Fiona M. Collier ◽  
Mark A. Kirkland ◽  
Ken Walder ◽  
Nicole Stupka
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Precursor Cells ◽  
Muscle Precursor ◽  
Muscle Precursor Cells

scholarly journals Isolation and Expansion of Muscle Precursor Cells from Human Skeletal Muscle Biopsies

2016 ◽  
pp. 195-204 ◽  
Author(s):  
Chiara Franzin ◽  
Martina Piccoli ◽  
Luca Urbani ◽  
Carlo Biz ◽  
Piergiorgio Gamba ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Precursor Cells ◽  
Muscle Precursor ◽  
Muscle Precursor Cells ◽  
Muscle Biopsies

scholarly journals Vitamin D receptor protein is associated with interleukin-6 in human skeletal muscle

Endocrine ◽  
2014 ◽  
Vol 49 (2) ◽  
pp. 512-520 ◽  
Author(s):  
Rachele M. Pojednic ◽  
Lisa Ceglia ◽  
Alice H. Lichtenstein ◽  
Bess Dawson-Hughes ◽  
Roger A. Fielding
Keyword(s):  
Skeletal Muscle ◽  
Vitamin D ◽  
Vitamin D Receptor ◽  
Interleukin 6 ◽  
Human Skeletal Muscle ◽  
Receptor Protein

Analysis of the callipyge phenotype through skeletal muscle development; association of Dlk1 with muscle precursor cells

2008 ◽  
Vol 76 (3) ◽  
pp. 283-298 ◽  
Author(s):  
Jason D. White ◽  
Tony Vuocolo ◽  
Matthew McDonagh ◽  
Miranda D. Grounds ◽  
Gregory S. Harper ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Development ◽  
Precursor Cells ◽  
Skeletal Muscle Development ◽  
Muscle Precursor ◽  
Muscle Precursor Cells

scholarly journals N-cadherin Promotes the Commitment and Differentiation of Skeletal Muscle Precursor Cells

1997 ◽  
Vol 185 (1) ◽  
pp. 14-24 ◽  
Author(s):  
Mindy George-Weinstein ◽  
Jacquelyn Gerhart ◽  
Jennifer Blitz ◽  
Eileen Simak ◽  
Karen A. Knudsen
Keyword(s):  
Skeletal Muscle ◽  
Precursor Cells ◽  
Muscle Precursor ◽  
Muscle Precursor Cells

Deficient leukemia inhibitory factor signaling in muscle precursor cells from patients with type 2 diabetes

2012 ◽  
Vol 303 (2) ◽  
pp. E283-E292 ◽  
Author(s):  
Christa Broholm ◽  
Claus Brandt ◽  
Ninna S. Schultz ◽  
Anders R. Nielsen ◽  
Bente K. Pedersen ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Leukemia Inhibitory Factor ◽  
Precursor Cells ◽  
Diabetic Patients ◽  
Healthy Individuals ◽  
Muscle Precursor ◽  
Muscle Precursor Cells

The cytokine leukemia-inhibitory factor (LIF) is expressed by skeletal muscle and induces proliferation of muscle precursor cells, an important feature of skeletal muscle maintenance and repair. We hypothesized that muscle precursor cells from patients with type 2 diabetes had a deficient response to LIF. The mRNA and protein expressions of LIF and its receptor (LIFR) were measured in skeletal muscle biopsies from healthy individuals and patients with type 2 diabetes by use of qPCR and Western blot. LIF signaling and response were studied following administration of recombinant LIF and siRNA knockdown of suppressor of cytokine signaling (SOCS)3 in myoblast cultures established from healthy individuals and patients with type 2 diabetes. Myoblast proliferation rate was assessed by bromodeoxyuridine incorporation. LIF and LIFR proteins were increased in both muscle tissue and cultured myoblasts from diabetic patients. Nonetheless, in the diabetic myoblasts, LIF-induced phosphorylation of signal transducer and activator of transcription (STAT)1 and STAT3 was impaired. The deficient response to LIF administration in the diabetic myoblasts was further emphasized by a lack of increase in LIF-stimulated cell proliferation and a decreased LIF-stimulated induction of the proliferation-promoting factors cyclin D1, JunB, and c-myc. SOCS3 protein was upregulated in diabetic myoblasts, and knockdown of SOCS3 rescued LIF-induced gene expression in diabetic myoblasts, whereas neither STAT1 or STAT3 signaling nor proliferation rate was affected. In conclusion, although LIF and LIFR proteins were increased in muscle tissue and myoblasts from diabetic patients, LIF signaling and LIF-stimulated cell proliferation were impaired in diabetic myoblasts, suggesting a novel mechanism by which muscle function is compromised in diabetes.

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