Induction of thermotolerance in early postimplantation rat embryos is associated with increased resistance to hyperthermia-induced apoptosis

Mirkes, Philip E.; Cornel, Leanne; Park, H. W.; Cunningham, M. L.

doi:10.1002/(sici)1096-9926(199709)56:3<210::aid-tera4>3.0.co;2-4

Cited by 35 publications

(13 citation statements)

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“…At higher elevations, the protection from the chaperones becomes inadequate and the heat shock response is activated to produce heat shock proteins that assist in restoring the structure and functions of the damaged proteins or the disposal of cells that have suffered irreparable protein degradation. The response has been studied in detail in rat embryos in culture (Mirkes,1985,1987; Walsh et al,1987,1989,1993,1994; Mirkes et al,1991,1997; Mirkes and Doggett,1992).…”

Section: Threshold Temperature Elevationsmentioning

confidence: 99%

“…The pathogenic effects of a damaging dose of heat at a sensitive period include cell death (Edwards et al,1974; Wanner et al,1976; Shiota,1988; Upfold et al,1989; Mirkes et al,1997; Breen et al,1999; Li and Shiota,1999), disruption of the normal sequence of gene activity that controls organogenesis (Shiota,1988; Li and Shiota,1999), and vascular disruption (Nilsen,1984). The severity of the defects depends on the thermal dose.…”

Section: The Special Sensitivity Of the Central Nervous Systemmentioning

confidence: 99%

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Review: Hyperthermia and fever during pregnancy

Edwards

2006

Birth Defects Research

226

155

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An episode of hyperthermia is not uncommon during pregnancy. The consequences depend on the extent of temperature elevation, its duration, and the stage of development when it occurs. Mild exposures during the preimplantation period and more severe exposures during embryonic and fetal development often result in prenatal death and abortion. Hyperthermia also causes a wide range of structural and functional defects. The central nervous system (CNS) is most at risk probably because it cannot compensate for the loss of prospective neurons by additional divisions by the surviving neuroblasts and it remains at risk at stages throughout pre- and postnatal life. In experimental animals the most common defects are of the neural tube, microphthalmia, cataract, and micrencephaly, with associated functional and behavioral problems. Defects of craniofacial development including clefts, the axial and appendicular skeleton, the body wall, teeth, and heart are also commonly found. Nearly all these defects have been found in human epidemiological studies following maternal fever or hyperthermia during pregnancy. Suggested future human studies include problems of CNS function after exposure to influenza and fever, including mental retardation, schizophrenia, autism, and cerebral palsy.

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Section: Threshold Temperature Elevationsmentioning

confidence: 99%

Section: The Special Sensitivity Of the Central Nervous Systemmentioning

confidence: 99%

Review: Hyperthermia and fever during pregnancy

Edwards

2006

Birth Defects Research

226

155

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“…The DNA fragmentation assay was carried out as described previously (Mirkes et al, 1997). Briefly, DNA was isolated from whole embryos or embryo parts (head, heart, and trunk) using Qiagen QIAamp Tissue kit according to manufacturer's instructions and the concentration determined by OD 260 measurement.…”

Section: Dna Fragmentation Assaymentioning

confidence: 99%

Teratogen-induced cell death in postimplantation mouse embryos: differential tissue sensitivity and hallmarks of apoptosis

Mirkes

Little

1998

Cell Death Differ

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Teratogen-induced cell death is a common event in the pathogenesis associated with tissues destined to be malformed. Although the importance of this cell death is recognized, little information is available concerning the biochemistry of teratogen-induced cell death. We show that three teratogens, hyperthermia, cyclophosphamide and sodium arsenite induce an increase in cell death in day 9.0 mouse embryos with concurrent induction of DNA fragmentation, activation of caspase-3 and the cleavage of poly (ADPribose) polymerase (PARP). Teratogen-induced cell death is also selective, i.e., some cells within a tissue die while others survive. In addition, cells within some tissues die when exposed to teratogens while cells in other tissues are relatively resistant to teratogen-induced cell death. An example of the latter selectivity is seen in the cells of the developing heart, which are resistant to the cytotoxic potential of many teratogens. We show that the absence of cell death in the heart is accompanied by the complete lack of DNA fragmentation, activtion of caspase-3 and the cleavage of PARP.

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“…Neural crest cells that are involved in the development of the outflow tracts of both ventricles, including the membranous and muscular septum, undergo apoptosis during normal development (Gittenberger‐De Groot et al, 2000). Animal models have demonstrated that various maternal exposures, including hyperthermia, diabetes, and retinoic acid, may functionally alter apoptosis, resulting in cardiac malformations (Edwards et al, 1997; Mirkes et al, 1997; Watanabe et al, 2001).…”

Section: Introductionmentioning

confidence: 99%