Corrigendum to “Laminin-511, inducer of hair growth, is down-regulated and its suppressor in hair growth, laminin-332 up-regulated in chemotherapy-induced alopecia”

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The author regrets that when this article was first published one of the references referred to an article that has been withdrawn from publication.

Please find the corrected text paragraphs from ‘Section 4’, plus the updated list of Refs. [34–37] below:

4. Discussion

CIA is thought to be caused by apoptotic cell death in hair matrix cells. The signals leading to apoptosis in CIA are thought to be p53, Fas (APO-1, CD95), Fas-associated death domain, caspase-8 and Bcl-2 [33–35]. In this regard, the down-regulation of laminin-511 that is induced by CYP may well contribute to activation of apoptosis of hair matrix cells. In fact, Hendrix et al. reported that in early and mid dystrophic catagen, TUNEL-positive cells appear around the DP, and after late dystrophic catagen, TUNEL-positive cells dramatically increased along the epithelial strand located in the lower part of hair follicle in the same CIA mouse model [9]. Cell–matrix interactions are essential for survival and proliferation of epithelial cells which undergo a specialized form of apoptosis termed anoikis when deprived for substrate attachment [36]. Thus, the loss of laminin-511 may trigger apoptotic pathways in hair matrix cells. In support of this possibility, here we have demonstrated that the number of TUNEL-positive cells in CYP-treated mice is decreased by treatment with a laminin-511-rich protein extract.

The results we present are consistent with emerging data indicating that laminin-511 is an essential and primary factor for both hair morphogenesis and anagen hair growth. Moreover, here we show that the effects of CYP exposure in mice can be partially overcome by injecting a laminin-511-rich protein extract into the back skin of treated mice. This leads to an obvious question. How does laminin-511 drive/support hair growth? Conti et al. reported that hair cycle progression is altered in α3-integrin-deficient grafted skin [37]. Thus one possibility is that laminin-511 may promote hair growth control through regulating the expression of α3 integrin. This notion is supported by our finding that the expression of laminin-511 was spatially and temporally well correlated with that of α3 integrin. Moreover, we also demonstrate that laminin-511 increase α3 integrin promoter activity in cultured keratinocytes. These findings lead us to speculate that the up-regulation of α3 integrin triggered by laminin-511 is inhibited by CYP treatment leading to CIA. In this regard, it should be noted that in our experiments, as laminin-332, a ligand for α3β1 integrin, is up-regulated following CYP. However, our preliminary studies do not indicate a role for laminin-332 in CIA since laminin-332 neutralizing antibodies do not appear to inhibit CIA nor does recombinant laminin-332 enhance the process.

References