Evidence for pathophysiological crosstalk between bones, cardiac, skeletal and smooth muscles

• DOI: 10.1096/fasebj.24.1_supplement.1046.8
• Publication Date: 2021-06-15T17:53:12Z
• Authors: Leticia Brotto; Neerupma Silswal; Chad Touchberry; Nikhil Parelkar; Robin Craig; Todd Hall; Michael Loghry; J Shen; C‐K Qu; Lynda Bonewald; Mark Johnson; Michael Wacker; Jon Andresen; Marco Brotto
• Keywords: Contractility; Crosstalk; Pathophysiology

We hypothesize that bone acts as an endocrine organ by sending regulatory signals to skeletal, smooth, and cardiac muscles reciprocally muscle regulates mass strength independent of mechanical loading. To test this hypothesis we measured in vitro contractility function intact aortas, cerebral arteries, hearts, skeletal muscles, determined tibial trabecular cortical BV/TV a mouse lacking specific phosphatase (MIP/MTMR14; MIPKO). Systemic ablation MIP induces intracellular elevation PI(3,5)P2 cells, leads gradual weakness accelerated aging directly associates with aberrant calcium homeostasis. observed 12–14 month old KO there were gender decreases cardiac, smooth but not BV/TV. These data support our are now investigating the mechanisms underlying pathophysiological crosstalk between bone. Since expression enzymatic activity decrease aged from wild type mice, could be involved sarcopenia, osteoporosis cardiovascular diseases. Support: Missouri Life Sciences Research Board Grant 09‐1101 MB, NIH‐NIAMS Grand Opportunities (GO) 1RC2AR058962‐01 LB, MJ, MB.