Expression of Heat Shock Proteins in Developing and Degenerating Rat Testes

Ogi, Shinsuke; Tanji, Nozomu; Iseda, Tokuhiro; Yokoyama, M.

doi:10.1080/014850199262454

Cited by 36 publications

(18 citation statements)

References 23 publications

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“…Heat-shock proteins, originally identified as heat-inducible gene products, are a family of highly conserved proteins that respond to a wide variety of stresses, including oxidative stress. Under oxidative stress, hepatic cells can produce high levels of stress response proteins, including HSPs, which protect against free radical insult (Liu et al 2015;Ogi et al 1999). In this study, protein levels of HSPs (except spot 281) were all induced in the high PFDoA dose group, indicating that a certain degree of oxidative stress might occur in rat liver exposed to PFDoA.…”

Section: Discussionmentioning

confidence: 71%

Activation of peroxisome proliferator-activated receptor α ameliorates perfluorododecanoic acid-induced production of reactive oxygen species in rat liver

et al. 2015

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Perfluorododecanoic acid (PFDoA) is a ubiquitous environmental pollutant known to cause hepatocellular hypertrophy; however, the mechanisms of hepatotoxicity remain poorly understood. In this study, male rats were exposed to 0, 0.05, 0.2 and 0.5 mg/kg/day of PFDoA for 110 days. After two-dimensional differential gel electrophoresis and MALDI-TOF/TOF analysis, 73 differentially expressed proteins involved in lipid metabolism, inflammation, stress response and other functions were successfully identified. Among them, six significantly changed proteins (CTE1, MTE1, HADHA, ECH1, ALDH2 and CPS1) were found to be regulated by peroxisome proliferator-activated receptor alpha (PPARα). The anti-oxidant enzyme activity assays of superoxide dismutase and glutathione peroxidase and the content of thiobarbituric acid-reactive substances in the liver implied that PFDoA caused oxidative stress. The mRNA levels of PPARα in rat primary hepatocytes were knocked down by lentivirus-mediated RNAi. Furthermore, targeted protein levels of CTE1 and MTE1 were down-regulated, while those of HADHA, ALDH2 and CPS1 were up-regulated. After PFDoA exposure, however, the targeted protein levels of CTE1 and ALDH2 increased compared with those of the knockdown untreated group. The reactive oxygen species (ROS) content in rat hepatocytes assayed by flow cytometry significantly increased in the PPARα knockdown groups, consistent with the PPARα antagonist GW6471- and agonist WY14643-treated groups. These results strongly suggested that PPARα played an important role in suppressing ROS content in hepatocytes following PFDoA exposure.

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Section: Discussionmentioning

confidence: 71%

Activation of peroxisome proliferator-activated receptor α ameliorates perfluorododecanoic acid-induced production of reactive oxygen species in rat liver

et al. 2015

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“…However, the increase in expression of these Hsps didn't prevent testicular cells from apoptosis, at least not in the C57BL/6 testis. The possible reasons are as follows: 1) The expression of Hsps is cell‐specific in testis (Meinhardt et al, 1995; Ogi et al, 1999; Aguilar‐Mahecha et al, 2001) so that the regulated transcription of Hsps may also be cell‐specific and cannot be discerned when whole testis was used for microarray analysis. 2) It has been recognized that HSPs regulate apoptosis differently; for example, HSP27 and HSP70 are antiapoptotic whereas HSP60 and HSP10 are proapoptotic.…”

Section: Discussionmentioning

confidence: 99%

Differential Gene Expression in the Testes of Different Murine Strains Under Normal and Hyperthermic Conditions

Liu

Zhou

Hively

et al. 2009

Journal of Andrology

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Cryptorchidism and scrotal heating result in abnormal spermatogenesis, but the mechanism(s) prescribing this temperature sensitivity are unknown. It was previously reported that the AKR/N or MRL/MpJ-+/+ mouse testis is more heat-resistant than the testis from the C57BL/6 strain. We have attempted to probe into the mechanism(s) involved in heat sensitivity by examining global gene expression profiles of normal and heat-treated testes from C57BL/6, AKR/N, and MRL/MpJ-+/+ mice by microarray analysis. In the normal C57BL/6 testis, 415 and 416 transcripts were differentially expressed (at least 2-fold higher or lower) when compared with the normal AKR/N and MRL/MpJ-+/+ testis, respectively. The AKR/N and MRL/MpJ-+/+ strains revealed 268 differentially expressed transcripts between them. There were 231 transcripts differentially expressed between C57BL/6 and 2 purported heat-resistant strains, AKR/N and MRL/MpJ-+/+. Next, the testes of C57BL/6 and AKR/N mice were exposed to 43°C for 15 minutes and harvested at different time points for terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) studies and microarrays. An increase of TUNEL-positive germ cell numbers was significant 8 hours after heat exposure in the C57BL/6 mouse. However, this increase was not observed in the AKR/N mouse until 10 hours after heat exposure. All tubules showed germ cell loss and disruption in C57BL/6 testis 24 hours after heat shock. In contrast, although a number of seminiferous tubules showed an abnormal morphology 24 hours post–heat shock in the AKR/N mouse, many tubules still retained a normal structure. Numerous transcripts exhibited differential regulation between the 2 strains within 24 hours after heat exposure. The differentially expressed transcripts in the testes 8 hours after heat exposure were targeted to identify the genes involved in the initial response rather than those attributable to germ cell loss. Twenty transcripts were significantly down-regulated and 19 genes were up-regulated by hyperthermia in C57BL/6 and did not show a parallel change in the AKR/N testis. Conversely, heat shock resulted in 30 up-regulated transcripts and 31 down-regulated transcripts in AKR/N that were not similarly regulated in C57BL/6. A number of genes shared similar differential expression patterns and differential regulation by hyperthermia in both strains of mice. Taken together, the results of the present study indicate that the diverse genetic backgrounds in the 3 strains lead to major differences in normal testis gene expression profiles, whereas the differences in heat shock responses involve a significantly smaller number of genes. The data generated may provide insights regarding gene networks and pathways involved in heat stress and their relationship to spermatogenesis.

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“…as occurs as with cryptorchidism or hot baths) as well as heat shock proteins whose levels are induced by hyperthermia. [4647]…”

Section: Proposed Mechanismsmentioning

confidence: 99%

Varicocele-induced infertility: Newer insights into its pathophysiology

Eisenberg

Lipshultz

2011

Indian J Urol

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The association between varicoceles and male infertility has been known since the 1950s; however, the pathophysiology of the process remains uncertain. The primary proposed hypotheses involve hyperthermia, venous pressure, testicular blood flow, hormonal imbalance, toxic substances, and reactive oxygen species. It is difficult to identify a single or dominant factor, and it is likely that many of these factors contribute to the infertile phenotype seen in clinical practice. Moreover, patient lifestyle and genetic factors likely affect patient susceptibilities to the varicocele insult. While the current studies have weaknesses, they provide building blocks for futures studies into the pathophysiology of the varicocele.

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Expression of Heat Shock Proteins in Developing and Degenerating Rat Testes

Cited by 36 publications

References 23 publications

Activation of peroxisome proliferator-activated receptor α ameliorates perfluorododecanoic acid-induced production of reactive oxygen species in rat liver

Activation of peroxisome proliferator-activated receptor α ameliorates perfluorododecanoic acid-induced production of reactive oxygen species in rat liver

Differential Gene Expression in the Testes of Different Murine Strains Under Normal and Hyperthermic Conditions

Varicocele-induced infertility: Newer insights into its pathophysiology

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