Apoptosis and necrosis during the circadian cycle in the centipede midgut

. 2016 Jul ; 253 (4) : 1051-61. [epub] 20150816

Jazyk angličtina Země Rakousko Médium print-electronic

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/pmid26277351
Odkazy

PubMed 26277351
DOI 10.1007/s00709-015-0864-8
PII: 10.1007/s00709-015-0864-8
Knihovny.cz E-zdroje

Three types of cells have been distinguished in the midgut epithelium of two centipedes, Lithobius forficatus and Scolopendra cingulata: digestive, secretory, and regenerative cells. According to the results of our previous studies, we decided to analyze the relationship between apoptosis and necrosis in their midgut epithelium and circadian rhythms. Ultrastructural analysis showed that these processes proceed in a continuous manner that is independent of the circadian rhythm in L. forficatus, while in S. cingulata necrosis is activated at midnight. Additionally, the description of apoptosis and necrosis showed no differences between males and females of both species analyzed. At the beginning of apoptosis, the cell cytoplasm becomes electron-dense, apparently in response to shrinkage of the cell. Organelles such as the mitochondria, cisterns of endoplasmic reticulum transform and degenerate. Nuclei gradually assume lobular shapes before the apoptotic cell is discharged into the midgut lumen. During necrosis, however, the cytoplasm of the cell becomes electron-lucent, and the number of organelles decreases. While the digestive cells of about 10 % of L. forficatus contain rickettsia-like pathogens, the corresponding cells in S. cingulata are free of rickettsia. As a result, we can state that apoptosis in L. forficatus is presumably responsible for protecting the organism against infections, while in S. cingulata apoptosis is not associated with the elimination of pathogens. Necrosis is attributed to mechanical damage, and the activation of this process coincides with proliferation of the midgut regenerative cells at midnight in S. cingulata.

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J Comp Physiol B. 2012 Aug;182(6):729-40 PubMed

Proc Natl Acad Sci U S A. 2011 Jul 19;108(29):12036-41 PubMed

Exp Oncol. 2012 Oct;34(3):146-52 PubMed

Arthropod Struct Dev. 2014 Jan;43(1):27-42 PubMed

Protoplasma. 2015 Sep;252(5):1387-96 PubMed

Arthropod Struct Dev. 2013 May;42(3):237-46 PubMed

Proc Natl Acad Sci U S A. 2011 Jun 28;108(26):10668-72 PubMed

Ecotoxicol Environ Saf. 2014 Mar;101:157-67 PubMed

Arthropod Struct Dev. 2012 May;41(3):271-9 PubMed

J Insect Physiol. 2007 Dec;53(12):1307-15 PubMed

Curr Opin Cell Biol. 1999 Dec;11(6):745-52 PubMed

Protoplasma. 2016 Mar;253(2):457-66 PubMed

Int J Radiat Biol. 1990 Jul;58(1):165-75 PubMed

Micron. 2002;33(7-8):647-54 PubMed

Apoptosis. 2010 Mar;15(3):293-312 PubMed

Tissue Cell. 2010 Feb;42(1):24-31 PubMed

Annu Rev Physiol. 2011;73:69-93 PubMed

J Immunol. 2003 Nov 1;171(9):4672-9 PubMed

J Insect Physiol. 2008 Feb;54(2):386-92 PubMed

FASEB J. 2005 Feb;19(2):304-6 PubMed

Mech Dev. 2007 Jan;124(1):23-34 PubMed

Autophagy. 2009 Aug;5(6):795-804 PubMed

Am Nat. 2007 May;169(5):632-46 PubMed

Apoptosis. 2012 Mar;17(3):305-24 PubMed

Micron. 2015 Jan;68:130-9 PubMed

Exp Cell Res. 2003 Feb 1;283(1):1-16 PubMed

Toxicol Pathol. 2007 Jun;35(4):495-516 PubMed

PLoS One. 2013 Nov 04;8(11):e79381 PubMed

Apoptosis. 2006 Sep;11(9):1643-51 PubMed

Infect Immun. 2005 Apr;73(4):1907-16 PubMed

Annu Rev Pharmacol Toxicol. 2001;41:367-401 PubMed

J Invertebr Pathol. 2007 Nov;96(3):244-54 PubMed

Int J Radiat Biol Relat Stud Phys Chem Med. 1988 May;53(5):717-27 PubMed

J Cell Mol Med. 2013 Jan;17(1):12-29 PubMed

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