Grapholita molesta （Busck） is a worldwide insect pest damaging stone and pome fruits. High temperature can significantly affect insect survival, development and fecundity. Heat shock protein （Hsp） genes were specu...Grapholita molesta （Busck） is a worldwide insect pest damaging stone and pome fruits. High temperature can significantly affect insect survival, development and fecundity. Heat shock protein （Hsp） genes were speculated to possess a pivotal function in response to high temperature stress. In this study, two full-length Hsp genes, Gmhsp90 and GmhspTO, were cloned from G. molesta using rapid amplification of complementary DNA ends （RACE）. The open reading frames of Gmhsp90 and Gmhsp70 obtained were 2 148 bp and 1 998 bp in length, respectively. Their deduced amino acids showed high homology to Hsp genes of other species. Subsequently, the transcriptional expression of Gmhsp90 and Gmhsp70 in G. molesta adults exposed at various temperatures （26, 29, 32, 35, 38, 41 and 44℃） for 1 h and at 41℃ for various time duration （0, 15, 30, 45, 60, 75, 90 and 105 min） were investigated via real time quantitative polymerase chain reaction （qPCR）. The relative expression levels of Gmhsp90 and Gmhsp70 in G. molesta adults were both up-regulated with the rise of temperature and time duration. In addition, the Gmhsp70 usually showed a higher transcription accumulation than Gmhsp90. Interestingly, Gmhsp90 and Gmhsp 70 in female adults could be induced much earlier than that in males, and the effective induction temperature in females was also lower than that in males. The distinct expression profiles of Gmhsp90 and Gmhsp 70 indicated that Gmhsp90 and Gmhsp 70 may play important roles in G. molesta adults responding to a thermal threat, and there is difference on induction between sexes.展开更多
Increasing evidence suggests that spinal micro- glia regulate pathological pain in males. In this study, we investigated the effects of several microglial and astroglial modulators on inflammatory and neuropathic pain...Increasing evidence suggests that spinal micro- glia regulate pathological pain in males. In this study, we investigated the effects of several microglial and astroglial modulators on inflammatory and neuropathic pain follow- ing intrathecal injection in male and female mice. These modulators were the microglial inhibitors minocycline and ZVEID （a caspase-6 inhibitor） and the astroglial inhibitors L-α-aminoadipate （L-AA, an astroglial toxin） and car- benoxolone （a connexin 43 inhibitor）, as well as U0126 （an ERK kinase inhibitor） and D-JNKI-1 （a c-Jun N-terminal kinase inhibitor）. We found that spinal administration of minocycline or ZVEID, or Caspase6 deletion, reduced formalin-induced inflammatory and nerve injury-induced neuropathic pain primarily in male mice. In contrast, intrathecal L-AA reduced neuropathic pain but not inflam- matory pain in both sexes. Intrathecal U0126 and D-JNKI- 1 reduced neuropathic pain in both sexes. Nerve injury caused spinal upregulation of the astroglial markers GFAP and Connexin 43 in both sexes. Collectively, our data confirmed male-dominant microglial signaling but also revealed sex-independent astroglial signaling in the spinal cord in inflammatory and neuropathic pain.展开更多
文摘Grapholita molesta （Busck） is a worldwide insect pest damaging stone and pome fruits. High temperature can significantly affect insect survival, development and fecundity. Heat shock protein （Hsp） genes were speculated to possess a pivotal function in response to high temperature stress. In this study, two full-length Hsp genes, Gmhsp90 and GmhspTO, were cloned from G. molesta using rapid amplification of complementary DNA ends （RACE）. The open reading frames of Gmhsp90 and Gmhsp70 obtained were 2 148 bp and 1 998 bp in length, respectively. Their deduced amino acids showed high homology to Hsp genes of other species. Subsequently, the transcriptional expression of Gmhsp90 and Gmhsp70 in G. molesta adults exposed at various temperatures （26, 29, 32, 35, 38, 41 and 44℃） for 1 h and at 41℃ for various time duration （0, 15, 30, 45, 60, 75, 90 and 105 min） were investigated via real time quantitative polymerase chain reaction （qPCR）. The relative expression levels of Gmhsp90 and Gmhsp70 in G. molesta adults were both up-regulated with the rise of temperature and time duration. In addition, the Gmhsp70 usually showed a higher transcription accumulation than Gmhsp90. Interestingly, Gmhsp90 and Gmhsp 70 in female adults could be induced much earlier than that in males, and the effective induction temperature in females was also lower than that in males. The distinct expression profiles of Gmhsp90 and Gmhsp 70 indicated that Gmhsp90 and Gmhsp 70 may play important roles in G. molesta adults responding to a thermal threat, and there is difference on induction between sexes.
基金supported by NIH R01 grants DE17794,DE22743,and NS87988 to RRJsupported by NIH T32 2T32GM008600a Foundation of Anesthesia Education and Research Fellowship
文摘Increasing evidence suggests that spinal micro- glia regulate pathological pain in males. In this study, we investigated the effects of several microglial and astroglial modulators on inflammatory and neuropathic pain follow- ing intrathecal injection in male and female mice. These modulators were the microglial inhibitors minocycline and ZVEID （a caspase-6 inhibitor） and the astroglial inhibitors L-α-aminoadipate （L-AA, an astroglial toxin） and car- benoxolone （a connexin 43 inhibitor）, as well as U0126 （an ERK kinase inhibitor） and D-JNKI-1 （a c-Jun N-terminal kinase inhibitor）. We found that spinal administration of minocycline or ZVEID, or Caspase6 deletion, reduced formalin-induced inflammatory and nerve injury-induced neuropathic pain primarily in male mice. In contrast, intrathecal L-AA reduced neuropathic pain but not inflam- matory pain in both sexes. Intrathecal U0126 and D-JNKI- 1 reduced neuropathic pain in both sexes. Nerve injury caused spinal upregulation of the astroglial markers GFAP and Connexin 43 in both sexes. Collectively, our data confirmed male-dominant microglial signaling but also revealed sex-independent astroglial signaling in the spinal cord in inflammatory and neuropathic pain.
