Sunday, October 10, 2010

Child Height Increase by inhibiting F-spondin

Previously, in the article on Alkaline Phosphatase we found that F-spondin antibodies increased height of rats by about 30%.  Now it's important to note that this was in organ cultures and not in a body where negative feedback mechanisms are present.  But 30% is huge.  A 30% increase on 69 inches(5'9") results in a height of about 90(7'6") inches.  What are the mechanisms in which F-spondin works and how can he inhibit F-spondin?

Plasmin-mediated release of the guidance molecule F-spondin from the extracellular matrix.

"Serine proteases are implicated in a variety of processes during neurogenesis, including cell migration, axon outgrowth, and synapse elimination. Tissue-type plasminogen activator and urokinase-type activator are expressed in the floor plate during embryonic development. F-spondin, a gene also expressed in the floor plate, encodes a secreted, extracellular matrix-attached protein that promotes outgrowth of commissural axons and inhibits outgrowth of motor axons[inhibit outgrowh of commissural axon and promote outgrowth of motor axons to grow taller?]. F-spondin is processed in vivo to yield an amino half protein that contains regions of homology to reelin and mindin, and a carboxyl half protein that contains either six or four thrombospondin type I repeats (TSRs). Plasmin cleaves F-spondin at its carboxyl terminus[inhibit plasmin to grow taller?]. By using nested deletion proteins and mutating potential plasmin cleavage sites, we have identified two cleavage sites, the first between the fifth and sixth TSRs, and the second at the fifth TSR. Analysis of the extracellular matrix (ECM) attachment properties of the TSRs revealed that the fifth and sixth TSRs bind to the ECM, but repeats 1-4 do not. Two basic motives are required to elicit binding of TSR module to the ECM. Plasmin releases the ECM-bound F-spondin protein."

Inhibiting motor axon growth and inhibiting plasmin may be a way to increase height in children.

"Metalloproteases, transforming growth factor-β, vascular endothelial growth factor, fibroblast growth factor, platelet-derived growth factor, and hepatic growth factor/scatter factor are produced as matrix-attached latent proteins, subjected to cleavage and subsequently to activation by plasmin" 

This us a clue that one of these factors inhibit growth.  We have metalloproteases, TGF-Beta(which is needed), VEGF(Released by Estrogen which gives the estrogen theory some weight), FGF, platelet-derived growth factor, and hepatic growth factor.  We also have plasmin inhibition as a way to increase height.

Here's a patent related to F-spondin by Steven B. Abramson


"F-spondin is a member of a family of proteins that collectively belong to a subgroup of TSR (thrombospondin) type I class molecules. F-spondin expression is significantly increased in osteoarthritic cartilage as well as in rodent meniscectomy models of OA. F-spondin has significant effects on human chondrocyte metabolism and is also expressed in the hypertrophic regions of embryonic growth plates where it acts to regulate mineralization and endochondral bone formation. F-spondin [may modulate] collagen degradation via unrecognized pathways that include activation of TGF-Beta and induction of MMPs and F-spondin [may induce] hypertrophic differentiation of articular chondrocytes and plays an essential role in the regulation of mineralization and endochondral bone formation. [We will] identify MMPs induced by F- spondin and examine their role in F-spondin-mediated collagen degradation[thus we can find which MMPs inhibit height growth], establish the role of TGF-Beta in modulation of F-spondin functions and compare functional activity of the full length F-spondin molecule relative to its proteolytic fragments. We will identify and characterize the interacting proteins of F-spondin:  investigate the interaction of F-spondin with the Latency-associated peptide (LAP) of the latent TGF-Beta complex and identify novel F- spondin binding proteins (proteases, receptors, matrix molecules) that may regulate its activity in articular cartilage. We will investigate F-spondin expression in cartilage in vivo iduring endochondral bone development. We will generate an F-spondin knockout mouse and characterize the changes in cartilage phenotype during endochondral bone development."

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