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Jon E. Wergedal

Researcher at Loma Linda University

Publications -  147
Citations -  8722

Jon E. Wergedal is an academic researcher from Loma Linda University. The author has contributed to research in topics: Bone density & Osteoblast. The author has an hindex of 55, co-authored 147 publications receiving 8404 citations. Previous affiliations of Jon E. Wergedal include United States Department of Veterans Affairs & Veterans Health Administration.

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Fluoride directly stimulates proliferation and alkaline phosphatase activity of bone-forming cells.

TL;DR: Treatment with sodium fluoride increased proliferation and alkaline phosphatase activity of bone cells in vitro and increasedBone formation in embryonic calvaria at concentrations that stimulate bone formation in vivo.
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Androgens directly stimulate proliferation of bone cells in vitro

TL;DR: It is concluded that androgens can stimulate human and murine osteoblastic cell proliferation in vitro, and induce expression of the osteoblast-line differentiation marker ALP, presumably by an androgen receptor mediated mechanism.
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Isolation of an inhibitory insulin-like growth factor (IGF) binding protein from bone cell-conditioned medium: a potential local regulator of IGF action

TL;DR: It is concluded that In-IGF-BP is a protein that has a unique sequence and significant biological actions on bone cells that is homogeneous and unique by the following criteria.
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A New Standard Genetic Map for the Laboratory Mouse

TL;DR: This work revisited high-resolution genetic map data from a large heterogeneous mouse population and constructed a revised genetic map of the mouse genome, incorporating 10,195 single nucleotide polymorphisms using a set of 47 families comprising 3546 meioses, providing a different picture of recombination in the mouse from that reported previously.
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TNF-related weak inducer of apoptosis (TWEAK) is a potent skeletal muscle-wasting cytokine

TL;DR: The data suggest that TWEAK induces skeletal muscle atrophy through inhibition of the PI3K/Akt signaling pathway and activation of the ubiquitin‐proteasome and NF‐kB systems.