Transforming growth factor Beta

Ans. is ‘b’ i.e., Angiopoietins, TGF & PDGF

Angiogenesis

o Blood vessels formation in adults is known as angiogenesis or neovascularization. It can occur by two ways:‑

1) Angiogenesis from pre-existing blood vessels

             The major steps in this process are :-

i)           Vasodilatation by NO, and VEGF-induced increased permeability of the pre-existing vessel.

ii)          Preoteolytic degradation of basement membrane by metalloproteinases (MMPs) and disruption of cell­to-cell contact between endothelial cells by plasminogen activator.

iii)        Migration of endothelial cells towards angiogenic stimulus.

iv)        Proliferation of endothelial cells, just behind the leading front of migrating cells.

v)         Maturation of endothelial cells.

vi)        Recruitment of periendothelial cells (pericytes and vascular smooth muscle cells) to form the mature cells.

2) Angiogenesis from endothelial precursor cells (EPCs)

             EPCs can be recruited from the bone marrow into tissues to initiate angiogenesis.

Growth factors involved in the process of angiogenesis

o VEGF is the most important growth factor in adult tissues undergoing angiogenesis.

o The most important receptor for VEGF is VEGFR-2, a tyrosine kinase receptor.

o VEGF induces the migration of EPCs in the bone marrow, and enhances the proliferation and differentiation of these cells at sites of angiogenesis.

o FGF 2 can also stimulate endothelial cell proliferation, differentiation and migration.

o Newly formed vessels are fragile and need to become stabilized, which requires the recruitment of pericytes and smooth muscle cells (periendothelial cells). Angiopoietin I and 2 (Ang 1 & 2), PDGF and TGF-0 participate in stabilization process.

Remember

• VEGF transcription is regulated by the transcription factor HIF, which is induced by hypoxia.

Ans. is ‘a’ i.e., TGF-

Ans. is ‘d’ i.e., Anaphylaxis

Transforming Growth factor beta:

Transforming growth factor β (TGF- β) is the most important cytokine for the synthesis and deposition of connective tissue proteins.

It is produced by most of the cells in granulation tissue, including alternatively activated macrophages.

The levels of TGF-β in tissues are primarily regulated not by the transcription of the gene but by the posttranscriptional activation of latent TGF-β, the rate of secretion of the active molecule, and factors in the ECM, notably integrins, that enhance or diminish TGF-β activity.

TGF-β stimulates fibroblast migration and proliferation, increased synthesis of collagen and fibronectin, and decreased degradation of ECM due to inhibition of metalloproteinases.

TGF-β is involved not only in scar formation after injury but also in the development of fibrosis in lung, liver, and kidneys that follows chronic inflammation.

TGF-β is also an antiinflammatory cytokine that serves to limit and terminate inflammatory responses. It does this by inhibiting lymphocyte proliferation and the activity of other leukocytes.

Ans. is ‘a’ i.e., TGF beta