Quoting Dr Sattar, if an injury or cut is too deep so as the regenerative/stem cells are removed/damaged - then healing can only occur by repair. Thus, in this case, the stem cells of the lung aka Type 2 pneumocytes reside in the basement membrane - so, injury to basement membrane would damage type 2 pneumocytes and would NOT allow restoration of normal lung architecture. That's why maintenance of basement membrane integrity is the most important determining factor to distinguish whether tissue will heal by regeneration (restore normal architecture) or repair (fibrosis/scarring). Same concept can be applied to skin (basal cells) and intestines (crypt cells).
You have to think about it this way: the basement membrane is the “scaffolding” on which [restorative] healing occurs. So, yes, stem cells (type II pneumocytes) would be involved in that healing process but they couldn’t restore the normal architecture (“no abnormalities”) without the ‘skeleton’ of the basement membrane telling them where to go, in what direction to grow, which way is “up”, etc. If the basement membrane is destroyed, you can still get healing, but it won’t be organized healing -- it’ll be disorganized healing, which does not appear as normal tissue. (Disorganized healing is better than no healing, but without a BM, the regenerating cells don’t have any “direction” and therefore can’t restore the normal architecture.)
I would think resolution involves the stem cells (type II pneumocytes). Is the intact basement membrane the answer because it limits spread?
can anyone explain why (D) metaplasia is incorrect?
submitted by ∗bubbles(79)
Basement membrane integrity is the determinant of full lung recovery following pulmonary insult.
Summary:
(1) loss of basement membrane integrity is critical in determining the “point of no return,” and contributes to the inability to reestablish normal lung architecture with promotion of fibrosis;
(2) loss of epithelial cells, endothelial cells, and basement membrane integrity in usual interstitial pneumonia associated with idiopathic pulmonary fibrosis leads to destroyed lung architecture and perpetual fibrosis;
(3) transforming growth factor-β is necessary, but not entirely sufficient, to promote permanent fibrosis;
(4) persistent injury/antigen/irritant is critical for the propagation of fibrosis;
(5) idiopathic pulmonary fibrosis is an example of a process related to the persistence of an “antigen(s),” chronic inflammation, and fibrosis; and
(6) unique cells are critical cellular players in the regulation of fibrosis.
citation: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/