Molecular Mechanism : Aspects Of Specificity And Regulation Elucidated Essay

Molecular Mechanism : Aspects Of Specificity And Regulation Elucidated Essay

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Kringle 5
(Angiostatin’s molecular mechanism: aspects of specificity and regulation elucidated)

Interaction of K5 with its receptor, the voltage-dependent anion channel interferes with both cytosolic intracellular free Ca2+ signalling and pH regulation in HUVEC

Angiogenesis and repair of blood vessels was preceded by increases in cytosolic pH in EC

Interference of these mechanisms by K5 may be the basis of its anti-angiogenic activity

Angiogenesis and Angiostatin 1v1
(Angiostatin’s molecular mechanism: aspects of specificity and regulation elucidated)

At low extracellular pH, angiostatin affects EC intracellular pH

Tumour extracellular pH is 5.6-7.6
Normal tissue is 7.2-7.6

Angiostatin is more potent at low extracellular pH

Therefore, angiogenesis and the acidic environment is induces are key to enhancing the activity of angiostatin

Angiostatin has a profound effect in vitro on intracellular pH in EC

pH regulating transporters that are active at low pH include the sodium proton exchanger, and the H+ linked monocarboxylate exchanger

Angiostatin treatment catalyzes FAK phosphorylation in the absence of integrin clustering

Integrin clustering is required for cell attachment to substrate

Attachment otoa substrate such as fibronectin causes integrins to form tetramers, and FAK is phosphorylated, inducing cytoskeletal elements to form structurally organized arrays that promote cell spreading and activating the NHE

The pH and oxygen levels are low, and the degree of attachment is compromised because cells are rapidly dividing and often motile, and the NHE is more active

Various integrin isoforms are expressed differently in tumours relative to normal tissue

Receptor distribution is modulated by matrix composition and ext...

... middle of paper ...

... No change in c-Myc was observed when cells were treated with angiostatin in SF (Figure 3F). We conclude that certain factors present in CM contribute to the increase of TSP in media. Overall, these data indicate that an increase in TSP-1 is associated with a decrease of c-Myc in tumors, consistent with previous published reports.26,27 (Figure 2A).



Angiostatin inhibits migration of host macrophages to the tumor
Bone marrow–derived cells that infiltrate tumors and differentiate into macrophages are called tumor-associated macrophages. Migration and infiltration of macrophages are hallmarks of tumor growth.28–30 Tumor-associated macrophages release several angiogenic factors, including MMP-9, VEGF, and IL-8.
Immunohistochemical analysis of mouse tumors showed reduced macrophage infiltration in angiostatin-treated mice relative to sham-treated controls.

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