Chronic whole-body heat treatment relieves atherosclerotic lesions, cardiovascular and metabolic abnormalities, and enhances survival time restoring the anti-inflammatory and anti-senescent heat shock response in mice

Mesocarp softening during papaya (Carica papaya L.) ripening was impaired by heating at 42C for 30 min followed by 49C for 70 min, with areas of the flesh failing to soften. Disruption of the softening process varied with stage of ripeness and harvest date. The respiratory climacteric and ethylene production were higher and occurred 2 days sooner in the injured fruit than in the noninjured fruit that had been exposed to 49C for only 30 min. Skin degreening and internal carotenoid synthesis were unaffected by the heat treatments. Exposure of ripening fruit to either 42C for 4 hr or 38 to 42C for 1 hr followed by 3 hr at 22C resulted in the development of thermotolerance to exposure to the otherwise injurious heat treatment of 49C for 70 min. Four stainable polypeptide bands increased and seven declined in single-dimensional acrylamide gels following incubation of fruit at the nondamaging temperature of 38C for 2 hr. Three polypeptides showed marked increases when polysomal RNA was translated. These polypeptides had apparent molecular weights of 17, 18, and 70 kDa. Proteins with molecular weights of 46, 54, and 63 kDa had slight increases after heat treatment. The levels of these polypeptides peaked 2 hr after heat treatment and declined within 24 hr. The amount of these polypeptides in the unheated control varied with the batch of fruit. The concentration of three translated polypeptides, with apparent molecular weights of 26, 37, and 46 kDa, declined. Other polypeptides continued to be translated during and after holding papayas for 2 hr at 38C.

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Starved Tetrahymena thermophila cells that are unable to mount an effective heat shock response selectively degrade their rRNA.

Molecular and Cellular Biology ◽

10.1128/mcb.4.10.2170 ◽

1984 ◽

Vol 4 (10) ◽

pp. 2170-2179 ◽

Cited By ~ 10

Author(s):

R L Hallberg ◽

K W Kraus ◽

R C Findly

Keyword(s):

Heat Treatment ◽

Heat Shock ◽

Heat Shock Response ◽

Nutrient Medium ◽

Tetrahymena Thermophila ◽

Mrna Metabolism ◽

Shock Response ◽

Reduced Rate ◽

Shock Proteins ◽

Rrna Degradation

Tetrahymena thermophila cells that had been shifted from log growth to a non-nutrient medium (60 mM Tris) were unable, during the first few hours of starvation, to mount a successful heat shock response and were killed by what should normally have been a nonlethal heat shock. An examination of the protein synthetic response of these short-starved cells during heat shock revealed that whereas they were able to initiate the synthesis of heat shock proteins, it was at a much reduced rate relative to controls and they quickly lost all capacity to synthesize any proteins. Certain pretreatments of cells, including a prior heat shock, abolished the heat shock inviability of these starved cells. Also, if cells were transferred to 10 mM Tris rather than 60 mM Tris, they were not killed by the same heat treatment. We found no abnormalities in either heat shock or non-heat shock mRNA metabolism in starved cells unable to survive a sublethal heat shock when compared with the response of those cells which can survive such a treatment. However, selective rRNA degradation occurred in the nonsurviving cells during the heat shock and this presumably accounted for their inviability. A prior heat shock administered to growing cells not only immunized them against the lethality of a heat shock while starved, but also prevented rRNA degradation from occurring.

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Histamine Is an Inducer of the Heat Shock Response in SOD1-G93A Models of ALS

International Journal of Molecular Sciences ◽

10.3390/ijms20153793 ◽

2019 ◽

Vol 20 (15) ◽

pp. 3793 ◽

Cited By ~ 2

Author(s):

Savina Apolloni ◽

Francesca Caputi ◽

Annabella Pignataro ◽

Susanna Amadio ◽

Paola Fabbrizio ◽

...

Keyword(s):

Heat Shock ◽

Motor Neuron ◽

Motor Neurons ◽

Heat Shock Response ◽

Type I ◽

Spine Density ◽

Shock Response ◽

Anti Inflammatory

(1) Background: Amyotrophic lateral sclerosis (ALS) is a multifactorial non-cell autonomous disease where activation of microglia and astrocytes largely contributes to motor neurons death. Heat shock proteins have been demonstrated to promote neuronal survival and exert a strong anti-inflammatory action in glia. Having previously shown that the pharmacological increase of the histamine content in the central nervous system (CNS) of SOD1-G93A mice decreases neuroinflammation, reduces motor neuron death, and increases mice life span, here we examined whether this effect could be mediated by an enhancement of the heat shock response. (2) Methods: Heat shock protein expression was analyzed in vitro and in vivo. Histamine was provided to primary microglia and NSC-34 motor neurons expressing the SOD1-G93A mutation. The brain permeable histamine precursor histidine was chronically administered to symptomatic SOD1-G93A mice. Spine density was measured by Golgi-staining in motor cortex of histidine-treated SOD1-G93A mice. (3) Results: We demonstrate that histamine activates the heat shock response in cultured SOD1-G93A microglia and motor neurons. In SOD1-G93A mice, histidine augments the protein content of GRP78 and Hsp70 in spinal cord and cortex, where the treatment also rescues type I motor neuron dendritic spine loss. (4) Conclusion: Besides the established histaminergic neuroprotective and anti-inflammatory effects, the induction of the heat shock response in the SOD1-G93A model by histamine confirms the importance of this pathway in the search for successful therapeutic solutions to treat ALS.

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