Coupling activation of pro-apoptotic caspases with autophagy in the Meckel´s cartilage

Title:

Coupling activation of pro-apoptotic caspases with autophagy in the Meckel´s cartilage

Creator:

Bíliková, P. , Švandová, E. , Veselá, B. , Doubek, J. , Poliard, A. , and Matalová, E.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:8a5e6a28-347c-4559-8a1c-8437edeed750
uuid:8a5e6a28-347c-4559-8a1c-8437edeed750
doi:10.33549/physiolres.933947

Subject:

cartilage, apoptosis, autophagy, caspase-2, and caspase-8

Type:

model:article and TEXT

Format:

bez média and svazek

Description:

Mammalian Meckel´s cartilage is a temporary structure associated with mandible development. Notably, its elimination is not executed by apoptosis, and autophagy was suggested as the major mechanism. Simultaneous reports point to pro-apoptotic caspases as novel participants in autophagic pathways in general. The aim of this research was to find out whether activation of pro-apoptotic caspases (-2, -3, -6, -7, -8 and -9) was associated with autophagy of the Meckel´s cartilage chondrocytes. Active caspases were examined in serial histological sections of mouse mandible using immunodetection and were correlated with incidence of autophagy based on Beclin-1 expression. Caspase-2 and caspase-8 were found in Beclin-1 positive regions, whereas caspase-3, -6, -7 and -9 were not present. Caspase-8 was further correlated with Fas/FasL and HIF-1α, potential triggers for its activation. Some Fas and FasL positivity was observed in the chondrocytes but caspase-8 activation was found also in FasL deficient cartilage. HIF-1α was abundantly present in the hypertrophic chondrocytes. Taken together, caspase-8 activation in the Meckel´s cartilage was demonstrated for the first time. Caspase-8 and caspase-2 were the only pro-apoptotic caspases detected in the Beclin-1 positive segment of the cartilage. Activation of caspase-8 appears FasL/Fas independent but may be switched on by HIF-1α.

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2019 Volume:68 | Number:1

Harvested from:

CDK

Metadata only:

false