Human CALM1(Calmodulin) ELISA Kit

Human osteoclasts were differentiated using receptor activator of NFB ligand (RANKL) and macrophage colony stimulating factor (M-CSF) from colony forming unit-granulocyte macrophage (CFU-GM) precursors of the myeloid lineage grown from umbilical cord blood. Gene expression profiling using quantitative polymerase chain reaction (Q-PCR) showed more than 1,000-fold induction of chemokine MCP-1 within 24h of RANKL treatment. MCP-1 mRNA content exceeds that of other assayed chemokines (CCL1, 3, 4, and 5) at all time points up to day 14 of treatment. MCP-1 induction preceded peak induction of calcium signaling activator calmodulin 1 (CALM1) and transcription factors JUN and FOS, which were at 3 days. Key osteoclast related transcription factors NFATc1 and NFATc2 showed peak induction at 7 days, while marker genes for osteoclast function cathepsin K and tartrate resistance acid phosphatase (TRAP) were maximally induced at 14 days, corresponding with mature osteoclast function. To test whether the early and substantial peak in MCP-1 expression is part of human osteoclast differentiation events, a dominant negative inhibitor of MCP-1 (7ND) was added simultaneously with RANKL and M-CSF, resulting in blockade of CALM1, JUN and NFATc2 induction and strong inhibition of human osteoclast differentiation. These data show that a cascade of gene expression leading to osteoclast differentiation depends on intact early MCP-1 induction and signaling in human osteoclasts. J. Cell. Biochem. 115: 303-312, 2014. (c) 2013 Wiley Periodicals, Inc.

Calcium overload, mediated by calmodulin (CaM), plays an important role in ischemia/reperfusion injury during acute ischemic brain damage. However, the regulation of CaM expression in cerebral ischemia is still not fully addressed. This study showed that the levels of plasma miR-335 were significantly down-regulated in 152 patients with acute cerebral infarction (0.60 +/- 0.31) compared to 136 age-matched healthy controls (1.16 +/- 0.30) (P < 0.01). Moreover, the levels negatively correlated with the National Institutes of Health Stroke Scale (NIHSS) scores in acute cerebral infarction patients (r = -0.680; P < 0.01). Transfection of miR-335 mimics and inhibitors inhibited CALM1 mRNA and CaM protein expressions in HUVECs. This study suggests that miR-335 is an important biomarker of acute cerebral infarction, and which functions are through regulating the expression of the CALM1 gene during acute ischemic brain injury. Our findings highlighted the potential of miR-335 as a target to develop agents to treat acute cerebral infarction.