Embryonic and maternal heat shock responses to a teratogenic hyperthermic insult

Bennett, Gregg; Mohl, Virginia K.; Finnell, Richard H.

doi:10.1016/0890-6238(90)90005-g

Cited by 17 publications

(6 citation statements)

References 26 publications

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“…Rat and mouse postimplantation embryos are capable of responding to heat stress with the induction of several HSPs (Mirkes, 1987;Walsh et al, 1987;Higo et al, 1989;Bennett et al, 1990;Honda et al, 1991), the most prominent being Hspa1a/a1b. Hspa1a/a1b can be induced in day 10 rat embryos (day 8.5 in mice) by temperatures above 408C.…”

Section: Introductionmentioning

confidence: 99%

Inducible 70 kDa heat shock proteins protect embryos from teratogen‐induced exencephaly: Analysis using Hspa1a/a1b knockout mice

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Dix

Mirkes

2009

Birth Defects Research

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These results show that embryos lacking the Hspa1a and Hspa1b genes are significantly more sensitive to hyperthermia-induced neural tube and eye defects, and this increased sensitivity is correlated with increased amounts of apoptosis. Thus, these results also suggest that Hspa1a and Hspa1b play an important role in protecting embryos from hyperthermia-induced congenital defects, possibly by reducing hyperthermia-induced apoptosis.

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Section: Introductionmentioning

confidence: 99%

Inducible 70 kDa heat shock proteins protect embryos from teratogen‐induced exencephaly: Analysis using Hspa1a/a1b knockout mice

Barrier

Dix

Mirkes

2009

Birth Defects Research

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“…As seen with Drosophila embryos, a similar heat‐shock response and induction of the heat‐shock proteins was reported to occur in mammalian embryos at temperatures that induced neural tube defects (Mirkes, 1987; Walsh et al, 1987; Bennett et al, 1990; Englen and Finnell, 1991; Finnell et al, 1992). Collectively, these studies demonstrated that heat induced the expression of the heat‐shock genes and proteins but the reduction in the normal protein synthesis was not as severe, or dramatic, as seen in Drosophila embryos.…”

Section: Mechanistic Observationsmentioning

confidence: 61%

“…DBA/2J embryos, which were totally resistant to heat‐induced neural tube defects, had a heat‐shock response that was short in duration. Although the heat‐shock proteins were induced by the hyperthermia treatment, normal protein synthesis resumed within 2 h. However, SWV embryos that were highly susceptible to a heat treatment had a much longer heat‐shock response, where the induction of HSPs lasted several hours and it took a longer time for normal protein synthesis to recommence (Bennett et al, 1990; Mohl et al, 1990; Englen and Finnell, 1991). Therefore, the induction of the typical heat‐shock, or stress, response did not correlate with either the susceptibility or occurrence of defects in a particular mouse strain.…”

Section: Mechanistic Observationsmentioning

confidence: 99%

Early experience in the application of distal protection devices in treatment of peripheral vascular disease of the lower extremities

Wholey

Toursarkissian

Postoak

et al. 2005

Cathet. Cardiovasc. Intervent.

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The objectives of this study were to reduce the risk of showering distal vessels with thromboemboli created during percutaneous interventions of the arteries in the lower extremities. Distal protection devices have been used in coronary and carotid interventions. Hence, using similar techniques, these filters and occlusion balloons were advanced past the targeted lesions and distally into femoral and popliteal arteries. Once opened, these devices allowed standard angioplasty and stent placement and captured the dislodged thromboemboli. Five cases were performed with the distal protection devices. One case used the distal occlusion balloon and four with the filter system. All five passed the lesion and were deployed. All five devices were retrieved without incident and were retrieved with substantial debris. There were no adverse events. The use of distal protection to treat high-risk or unstable lesions in the lower extremities shows great promise. Further case will be needed to evaluate the device for feasibility and safety.

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“…As seen with Drosophila embryos, a similar heat-shock response and induction of the heat-shock proteins was reported to occur in mammalian embryos at temperatures that induced neural tube defects (Mirkes, 1987;Walsh et al, 1987;Bennett et al, 1990;Englen and Finnell, 1991;Finnell et al, 1992). Collectively, these studies demonstrated that heat induced the expression of the heat-shock genes and proteins but the reduction in the normal protein synthesis was not as severe, or dramatic, as seen in Drosophila embryos.…”

Section: Mechanistic Observationsmentioning

confidence: 71%

Hyperthermia: malformations to chaperones

Bennett

2010

Birth Defects Research Pt B

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Hyperthermia has been known to induce malformations in numerous animal models as well being associated with human abnormalities. This was apparent particularly when the hyperthermia exposure was during the early stages of neural development. Although it was recognized relatively early that these exposures induced cell death, the specific molecular mechanism of how a brief heat exposure was translated in to specific cellular functions remains largely unknown. While our understanding of the events that govern how cells react to heat, or stresses in general, has increased, there is much that remains undiscovered. In this brief review, animal and clinical observations are outlined as are some of the scientific explorations that were undertaken to characterize, define, and better understand the morphological, biochemical, and molecular effects of hyperthermia on the developing embryo.

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Embryonic and maternal heat shock responses to a teratogenic hyperthermic insult

Cited by 17 publications

References 26 publications

Inducible 70 kDa heat shock proteins protect embryos from teratogen‐induced exencephaly: Analysis using Hspa1a/a1b knockout mice

Inducible 70 kDa heat shock proteins protect embryos from teratogen‐induced exencephaly: Analysis using Hspa1a/a1b knockout mice

Early experience in the application of distal protection devices in treatment of peripheral vascular disease of the lower extremities

Hyperthermia: malformations to chaperones

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