In the present work we studied whether two cell types in the TM, cribriform and corneoscleral cells, can be distinguished by differences in the expression of BM components. To answer this, we focused on three distinct questions: (1) which BM components are expressed by TM cells, (2) what are the differences in the expression profiles between corneoscleral and cribriform TM cells, and (3) do these two cell types respond differently to TGF-β2? We examined four components of BM: collagen IV, laminin, nidogen, and collagen VIII. Collagen type IV chains α1 and α2 are ubiquitous BM components forming a cross-linked scaffold in mature basal laminae.
10 11 12 In contrast, the incorporation of α3, α4, α5, or α6 chains is variable and apparently linked to functional features of specialized BMs.
11 12 13 14 Mutations in the genes coding for these chains correlate with genetic diseases like Alport syndrome, Goodpasture syndrome, and leiomyomatosis, causing severe organ- or tissue-specific dysfunction.
11 15 16 17 18 19 20 21 Pathogenic mutations in just one of these genes may lead to the absence of the other isoforms within the BM, suggesting dependency of expression among them.
16 17 In contrast, however, in the α3 knockout mouse, expression of the α4, α5, and α6 chains was detectable, which contradicts a coupled expression mechanism.
13 20 In our study, cribriform and corneoscleral TM cells expressed the α1, α2, α4, α5, and α6 chains but not the α3 chain, supporting the knockout mouse data. The functional relevance of the α3 chain, however, is not known. In the anterior eye segment, α3 expression and deposition was shown in the specialized BMs of Descemet’s membrane and the lens capsule.
15 19 Of interest, at the transition from cornea to TM, α3 expression ends, and the tissue loses its transparency.