Cell death and survival alterations in Malpighian tubules of Triatoma infestans following heat shock

Citation
Mls. Mello et al., Cell death and survival alterations in Malpighian tubules of Triatoma infestans following heat shock, BIOC CELL B, 79(6), 2001, pp. 709-717
Citations number
29
Categorie Soggetti
Cell & Developmental Biology
Journal title
BIOCHEMISTRY AND CELL BIOLOGY-BIOCHIMIE ET BIOLOGIE CELLULAIRE
ISSN journal
08298211 → ACNP
Volume
79
Issue
6
Year of publication
2001
Pages
709 - 717
Database
ISI
SICI code
0829-8211(200112)79:6<709:CDASAI>2.0.ZU;2-5
Abstract
In this study, we examined cell survival and cell death in response to heat shock in an insect organ composed of highly polyploid cells no longer capa ble of cell division. For this, the frequency of nuclear phenotypes in Feul gen-stained Malpighian tubules of the blood-sucking insect, Triatoma infest ans, was analyzed at various times after a short heat shock with or without subsequent moderate fasting. Cell death DNA fragmentation was studied immu nocytochemically. Normal phenotypes and phenotypes indicative of cell survi val (heterochromatin decondensation, nuclear fusion) and death (apoptosis, necrosis) were observed, especially in heat-shocked specimens. While the nu mber of total and normal nuclei decreased following heat shock, the frequen cy of apoptosis increased during a short period (7 days) after heat shock. During a 30-day period following heat shock, the frequency of necrosis in f asted but not in fully nourished nymphs increased simultaneously with a dec rease in the frequency of apoptosis. This finding suggests that the stress promoted by heat shock, but not that associated with heat shock plus fastin g, can be dealt with by the apoptosis program. When considering the forms o f cell survival, heterochromatin decondensation was more relevant in fully nourished nymphs, whereas nuclear and cell fusions were more important in f asted specimens. The forms of cell survival and cell death reported here ma y have protected the organ from damage by the stressing agents. In cells wi th no induction or accumulation of heat-shock proteins, cell death and the forms of cell survival observed here were the probable consequence.