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Lecture 3

Physiology 4530A/B Lecture 3: Lecture 3

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Western University
Physiology 4530A/B
Frank Beier

LEC 3: Extraskeletal Ossification Similarities: - Formation of cartilage and bone where they shouldn’t form - Triggered by mech factors/trauma/inflamm - Unphysiological diff of specific cells - Skeleton-specific regulatory mechs as pot’l therapeutic targets Differences: - Underlying conditions (e.g. mutations for FOP, POH; lifestyle for v.c.) - Specific cells undergoing skeletal diff - Location in body - Specific outcomes: fatal in FOP; impairment in v.c. Vascular Calcification a) Amorphous vascular calcification: mineral accum without cellular changes b) Chondro-osseous vascular calcification: endochondral ossification of extraskeletal cartilage/bone due to change in phenotype in soft tissues (e.g. SM and epith cells) Clinical consequences: diastolic dysfunction, HT, ventricular hypertrophy, heart failure Driven by abnormalities: - Developmental: inappropriate re-establishment of developmental pathways - Inflammatory: e.g. obesity is constant inflamm so can trigger cell changes - Metabolic: poor nutrition, diabetes, excess/deficiency If you KO MGP, v.c. occurs. FOP Initial sign is a bone abnormality in big toe. Not much happens til trauma. Fatal because heterotopic ossification interferes w lung func and muscles can’t support it. Due to ACVR1 activating GoF mutation in IC domain, FGF receptor for BMP; - Normally, ACVR1 threonine receptor binds to BMP, phosphorylates SMADs, which forms heterodimers and then translocates to nucleus - Mutated:ACVR1 binds to other ligands like activin as well o Usually activin binds to type I and II receptor complex and acti
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