Corroborating evidence for aberrant expression of histone deacetylase 8 in endometriosis
Abstract Purpose The aim of this study was to evaluate the dynamic change in staining of Class I HDACs and Hdac6 in lesions harvested serially from different time points in mice with induced endometriosis. In addition, the effect of Hdac8 activation as well as Hdac8 and Hdac6 inhibition on lesional...
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| Format: | Article |
| Jezik: | English |
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Wiley
2023-01-01
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| Serija: | Reproductive Medicine and Biology |
| Teme: | |
| Online dostop: | https://doi.org/10.1002/rmb2.12527 |
| _version_ | 1827398911954780160 |
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| author | Hanxi Zheng Xishi Liu Sun‐Wei Guo |
| author_facet | Hanxi Zheng Xishi Liu Sun‐Wei Guo |
| author_sort | Hanxi Zheng |
| collection | DOAJ |
| description | Abstract Purpose The aim of this study was to evaluate the dynamic change in staining of Class I HDACs and Hdac6 in lesions harvested serially from different time points in mice with induced endometriosis. In addition, the effect of Hdac8 activation as well as Hdac8 and Hdac6 inhibition on lesional progression and fibrogenesis was evaluated. Methods Immunohistochemistry analysis of Class I HDACs and Hdac6 in serially harvested lesion samples in mouse. Hdac8 activation, as well as Hdac6/8 inhibition, was evaluated in mice with induced endometriosis. Results We found a progressive increase in lesional staining of Hdac1, Hdac8, and Hdac6 and gradual decrease in Hdac2 staining and consistently reduced staining of Hdac3 during the course of lesional progression. The stromal Hdac8 staining correlated most prominently with all markers of lesional fibrosis. Hdac8 activation significantly accelerated the progression and fibrogenesis of endometriotic lesions. In contrast, specific inhibition of Hdac8 or Hdac6, especially of Hdac8, significantly hindered lesional progression and fibrogenesis. Conclusions Hdac8 is progressively and aberrantly overexpressed as endometriotic lesions progress. This, along with the documented HDAC1 upregulation in endometriosis and the overwhelming evidence for the therapeutic potentials of HDACIs, calls for further and in‐depth investigation of epigenetic aberrations of endometriosis in general and of HDACs in particular. |
| first_indexed | 2024-03-08T19:35:47Z |
| format | Article |
| id | doaj.art-ce08a73ca6074c5ca344438541678cea |
| institution | Directory Open Access Journal |
| issn | 1445-5781 1447-0578 |
| language | English |
| last_indexed | 2024-03-08T19:35:47Z |
| publishDate | 2023-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Reproductive Medicine and Biology |
| spelling | doaj.art-ce08a73ca6074c5ca344438541678cea2023-12-26T04:30:44ZengWileyReproductive Medicine and Biology1445-57811447-05782023-01-01221n/an/a10.1002/rmb2.12527Corroborating evidence for aberrant expression of histone deacetylase 8 in endometriosisHanxi Zheng0Xishi Liu1Sun‐Wei Guo2Department of Gynecology Shanghai Obstetrics and Gynecology Hospital, Fudan University Shanghai ChinaDepartment of Gynecology Shanghai Obstetrics and Gynecology Hospital, Fudan University Shanghai ChinaShanghai Key Laboratory of Female Reproductive Endocrine‐Related Diseases Fudan University Shanghai ChinaAbstract Purpose The aim of this study was to evaluate the dynamic change in staining of Class I HDACs and Hdac6 in lesions harvested serially from different time points in mice with induced endometriosis. In addition, the effect of Hdac8 activation as well as Hdac8 and Hdac6 inhibition on lesional progression and fibrogenesis was evaluated. Methods Immunohistochemistry analysis of Class I HDACs and Hdac6 in serially harvested lesion samples in mouse. Hdac8 activation, as well as Hdac6/8 inhibition, was evaluated in mice with induced endometriosis. Results We found a progressive increase in lesional staining of Hdac1, Hdac8, and Hdac6 and gradual decrease in Hdac2 staining and consistently reduced staining of Hdac3 during the course of lesional progression. The stromal Hdac8 staining correlated most prominently with all markers of lesional fibrosis. Hdac8 activation significantly accelerated the progression and fibrogenesis of endometriotic lesions. In contrast, specific inhibition of Hdac8 or Hdac6, especially of Hdac8, significantly hindered lesional progression and fibrogenesis. Conclusions Hdac8 is progressively and aberrantly overexpressed as endometriotic lesions progress. This, along with the documented HDAC1 upregulation in endometriosis and the overwhelming evidence for the therapeutic potentials of HDACIs, calls for further and in‐depth investigation of epigenetic aberrations of endometriosis in general and of HDACs in particular.https://doi.org/10.1002/rmb2.12527endometriosisfibrogenesishistone deacetylase 8mouseprogression |
| spellingShingle | Hanxi Zheng Xishi Liu Sun‐Wei Guo Corroborating evidence for aberrant expression of histone deacetylase 8 in endometriosis Reproductive Medicine and Biology endometriosis fibrogenesis histone deacetylase 8 mouse progression |
| title | Corroborating evidence for aberrant expression of histone deacetylase 8 in endometriosis |
| title_full | Corroborating evidence for aberrant expression of histone deacetylase 8 in endometriosis |
| title_fullStr | Corroborating evidence for aberrant expression of histone deacetylase 8 in endometriosis |
| title_full_unstemmed | Corroborating evidence for aberrant expression of histone deacetylase 8 in endometriosis |
| title_short | Corroborating evidence for aberrant expression of histone deacetylase 8 in endometriosis |
| title_sort | corroborating evidence for aberrant expression of histone deacetylase 8 in endometriosis |
| topic | endometriosis fibrogenesis histone deacetylase 8 mouse progression |
| url | https://doi.org/10.1002/rmb2.12527 |
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