Mast Cells and Hemangioma

Abstract

Hemangioma is a primary tumor of the microvasculature in which angiogenesis is initially excessive, followed by spontaneous regression of the newly formed vessels, with the cellular parenchyma gradually being replaced with fibrofatty tissue. Mast cells, which are highly heterogenous in terms of their morphology, function, and metabolic products, have been implicated in the pathophysiology of hemangioma. Csaba stain shows that mast cells are predominantly of the biogenic amine phenotype throughout the development of hemangioma. The predominance of this phenotype remains unaltered following successful steroid therapy, although their number increases fourfold. Mast cells, all of which stain positive for tryptase, and those that stain positive for chymase as well, have been identified in hemangioma biopsy specimens throughout the three developmental phases. The total number of mast cells is highest during the involuting phase, less in the involuted phase, and least in the proliferative phase. The proportion of mast cells that contain both tryptase and chymase decreases from the proliferative through involuting to the involuted phase. This decreasing proportion of mast cells that contain both tryptase and chymase with ongoing involution parallels that of progressive deposition of the extracellular matrix as indicated by increasing fibrosis and fatty deposition. The short-chain type VIII collagen, thought to play a key role in angiogenesis, has been detected throughout the developmental phases of hemangioma. It has been postulated that this collagen, which is produced early in new vessel development, provides a substratum to facilitate the migration of endothelial cells. It may also facilitate the deposition of other extracellular constituents and influence cell movement and the maintenance of cell phenotypes. The intracellular localization of type VIII collagen in mast cells only in the early proliferative phase suggests that there is an active synthesis by mast cells during this phase. The increasing extracellular localization during hemangioma development may be caused by an increased secretion of protein from intracellular stores. The increased number of mast cells during the involuting phase indicates that these cells may play a role in the regression of hemangioma. This is in contrast to the large body of evidence showing the proangiogenic role of mast cells. The proportion of proliferating mast cells decreases, whereas the proportion of mast cells positive for clusterin/apolipoprotein J increases with ongoing involution of hemangioma. Clusterin/apolipoprotein J expression has been considered as a prominent marker of apoptotic cell loss. The presence of clusterin/apolipoprotein J granules both in the adjacent endothelial cells and in capillary lumens suggests that mast cells may be secreting this apoptotic modulator to promote the regression of hemangioma. Certain effectors produced by mast cells may participate in the development of hemangioma. It has been proposed that one of the functions of mast cells is to r...

siRNA‐targeted COL8A1 inhibits proliferation, reduces invasion and enhances sensitivity to D‐limonence treatment in hepatocarcinoma cells

“…Increasing evidence indicates that collagen type VIII plays a role in atherogenesis and vascular remodeling, presumably through modification of cell migration and proliferation (7,8). The short-chain type VIII collagen, thought to play a key role in angiogenesis, has been detected throughout the developmental phases of hemangioma (9). The COL8A1 gene encodes the alpha 1 chain of collagen, type VIII.…”

Mast cells and cutaneous malignancies

“…22 These wide-ranging biological characteristics, their ubiquitous distribution and strategic locations near blood vessels, nerves, inflamed tissues and neoplastic foci enable them to play a central role in a multitude of physiologic, immunologic and pathologic processes. 20,[23][24][25] We have recently reviewed the biology of mast cells. 25 The effects of mast cell mediators on the development and spread of cutaneous malignancies are likely to be mediated through multiple pathways, including immunosuppression, enhancement of angiogenesis, disruption of the extracellular matrix and promotion of tumor cell mitosis ( Figure 1).…”

“…20,[23][24][25] We have recently reviewed the biology of mast cells. 25 The effects of mast cell mediators on the development and spread of cutaneous malignancies are likely to be mediated through multiple pathways, including immunosuppression, enhancement of angiogenesis, disruption of the extracellular matrix and promotion of tumor cell mitosis ( Figure 1). …”

Myeloid Cells in Infantile Hemangioma

“…2 Mast cells have been proposed to have a role in hemangioma progression 3 as have endothelial progenitor cells. 4 Hemangioma endothelial cells were shown to express the lymphatic endothelial marker LYVE-1, suggesting that these cells are arrested in an early vascular differentiation state.…”