Fibrodysplasia ossificans progressiva (FOP) is a rare autosomal dominant disorder characterized by congenital malformation of the great toes and by progressive heterotopic bone formation in muscle tissue. Recently, a mutation involving a single amino acid substitution in a bone morphogenetic protein (BMP) type I receptor, ALK2, was identified in patients with FOP. We report here that the identical mutation, R206H, was observed in
a b s t r a c tRecent studies have indicated that acetylcholine (ACh) plays a vital role in various tissues, while the role of ACh in bone metabolism remains unclear. Here we demonstrated that ACh induced cell proliferation and reduced alkaline phosphatase (ALP) activity via nicotinic (nAChRs) and muscarinic acetylcholine receptors (mAChRs) in osteoblasts. We detected mRNA expression of several nAChRs and mAChRs. Furthermore, we showed that cholinergic components were up-regulated and subunits/subtypes of acetylcholine receptors altered during osteoblast differentiation. To our knowledge, this is the first report demonstrating that osteoblasts express specific acetylcholine receptors and cholinergic components and that ACh plays a possible role in regulating the proliferation and differentiation of osteoblasts. Crown
The aim of this study was to compare the multidimensional properties among subtypes of painful temporomandibular disorders (TMD): myofascial pain (group I), disc displacement (group II), arthralgia (group IIIa) and osteoarthritis (group IIIb). A total of 511 patients answered a battery of questionnaires, which included questions relating to intensity and duration of pain, the Japanese version of the McGill Pain Questionnaire, limitation of daily functions, the Hospital Anxiety and Depression Scale, the Eysenck Personality Questionnaire short-form and 34 items of behavioural contributing factors. Group IIIb showed significantly the highest age in all subtypes. Those in group I had higher depression scores than those in group II (P = 0.005). Group IIIa had a lower women's ratio than in group II (P = 0.001) and the patients showed a shorter pain duration than those in groups I (P = 0.000) and II (P = 0.001). Group IIIa patients also showed lower visual analogue scale (VAS) ratings for pain descriptors 'heavy' (P = 0.002) and 'tiring' (P = 0.004) than those of group I, and 'dull' (P = 0.005), 'heavy' (P = 0.001) and 'tiring' (P = 0.005) than those of group II. Group IIIa showed lower ratios of contributing factors of 'an awareness of grinding/clenching during sleep' (P = 0.000) and 'an awareness of clenching sensation when waking up at night' (P = 0.002) than those of group I, and also showed a higher ratio of 'a liking for a hard food' (P = 0.000) and lower ratio of 'talking for a long time on the telephone' (P = 0.001) than those of group II. In conclusion, although several properties were different between subtypes, the majority of them were similar in the four subtypes of TMD.
Bone morphogenetic proteins (BMPs) induce ectopic bone formation in muscle tissue in vivo and convert myoblasts such that they differentiate into osteoblastic cells in vitro. We report here that constitutively active Smad1 induced osteoblastic differentiation of C2C12 myoblasts in cooperation with Smad4 or Runx2. In floxed Smad4 mice-derived cells, Smad4 ablation partially suppressed BMP-4-induced osteoblast differentiation. In contrast, the BMP-4-induced inhibition of myogenesis was lost by Smad4 ablation and restored by Smad4 overexpression. A nuclear zinc finger protein, E4F1, was identified as a possible component of the Smad4 complex that suppresses myogenic differentiation in response to BMP signaling. In the presence of Smad4, E4F1 stimulated the expression of Ids. Taken together, these findings suggest that the Smad signaling pathway may play a dual role in the BMP-induced conversion of myoblasts to osteoblastic cells.
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