The part of the Type II small cavi...

The part of the Type II small cavity in Lung Function and Repair

from one side of to the other the past 15 years, investigations of the metabolism and solitary abode; squalid biology of the lung have joined those of more classic aspects of pulmonary physiology as significant constituents of the literature on pulmonary biology and medicine. This broadening of emphasis in pulmonary research ponders the recognition that both the metabolic and gas exchange activities of the lung determine the overall physiologic functions of the tissue. Ultimately, these functions must be accounted for at the cellular and molecular plains if a complete understanding of the mechanisms of pulmonary disease is to be attained. This article is intended to address single aspect of this complex cellular biology, the factors which affect the differentiation of emblem II pneumocytes in the alveolar epithelium. More specifically, the part of the extracellular matrix in the determination of impressed sign II cell differentiation and the functional significance of the interaction of these pneumocyte with the matrix will be considered.

The distal parenchymal or alveolar region of the human lung is comprised of five major small cavity populations.[1] These include types I and II epithelial small rooms a heterogeneous population of interstitial enclosed spaces endothelial cells, and alveolar macrophages. The greatest proportion of the alveolar surface is overlayed by type I epithelial solitary abode; squalids which account for 93 percent of the proximal aspect of the barrier to gas exchange. emblem II epithelial cells, which are half as numerous as their prototype I counterparts, occupy the remainder of the alveolar surface. Although archetype II cells likely make no other than a minor contribution to the pathway for gas exchange,[1,2] one as well as the other their metabolic and progenitor functions are required to maintain normal pulmonary function.[3]

Substantial damage to the impressed sign I epithelium is observed following a variety of insults to the lung These injurious conditions include frontage to nitrogen dioxide,[4,5] hyperoxia [69] and oleic acid.[10] The pathophysiology and consecutions of such damage have been studied chiefly extensively in animal models, and it is these investigations which support the part of alveolar type II small rooms in the repair of acute lung injury. In the late 1960 the ultrastructural and morphometric data of Kapanci et al[7] indicated that representation II cell hyperplasia plays a significant part in restoration and repair of the alveolar surface following oxygen injury to the lung of monkeys[6] Later work through Evans et al[4,5] and according to Adamson and Bowden[8] confirmed that representation II cell growth and division, coupl with phenotypic changes in a portion of the resulting small cavity population, play an important character in the renewal of protoplast I epithelium as well as in normal lung development[9]

Characteristics of the Differentiated sign II Cell

following to definition of the general cellular changes which succeed acute injury, there has been a considerable sprouting of interest in the character of the type II lonely dwelling in this process. Because this rejoinder involves cell growth and division, along with a transition of the emblem II cell to a prototype I phenotype, progress in this area has required that specific, quantifiable indices of the amplitude of type II cell differentiation be identified and validated. These characteristics have serv as markers to allow more direct evaluation of the actions of specific biologic and biochemical factors to favor retention or los of emblem II cell differentiation.

Table 1 summarizes a certain number of of the morphologic, biochemical, and metabolic characteristics of the differentiated shadow II cell. The typical stamp II cell is located in the corner of the alveolus, encircleed by its junctions with the token I epithelium.[11] Any given solitary abode; squalid may have exposure on more than individual alveolar surface[12] toward which it reach outs multiple microvilli. On the ultrastructural even the cytoplasm is rich in organelles including mitochondria, uncut endoplasmic reticulum, and golgi.[11,12] mostly typical of the type II confined apartment ultrastructure are the lamellar bodies, multilamellar vesicles containing concentric phospholipid lamellae, which play a character in the production of the major symbol II cell product pulmonary surfactant.[13] In conjunction with the surfactant pathway, the emblem II cell demonstrates high activity of the enzyme required for phospholipid biosynthesis[14] and is active in the production of the major lipid constituents of surfactant, particularly disaturated phosphatidylcholine (DSPC)[13] the two the production and secretion of surfactant constitutings are subject to hormonal regulation.[13] Release of the peace of the lamellar bodies to the alveolar surface is sensitive to hormonal and mechanical stimuli.[15] The small cavitys express both the messenger RNA and protein results of the genes for the surfactant-associated apoproteins.[16,17] Typically, the differentiated stamp II pneumocyte demonstrates little or no proliferative activity and small in number cells contain mitotic figures. Incorporation of radiolabeled thymidine (TdR) into cellular DNA is minimal in vivo and in freshly isolated small cavitys in primary culture.[18,19]