Inhibition of miR-155 Promotes TGF-β Mediated Suppression of HIV Release in the Cervical Epithelial Cells
TGF-β has been shown to play a differential role in either restricting or aiding HIV infection in different cell types, however its role in the cervical cells is hitherto undefined. Among females, more than 80% of infections occur through heterosexual contact where cervicovaginal mucosa plays a crit...
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| Format: | Article |
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MDPI AG
2021-11-01
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| Series: | Viruses |
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| Online Access: | https://www.mdpi.com/1999-4915/13/11/2266 |
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| author | Jyotsna Gokavi Sharwari Sadawarte Anant Shelke Urmila Kulkarni-Kale Madhuri Thakar Vandana Saxena |
| author_facet | Jyotsna Gokavi Sharwari Sadawarte Anant Shelke Urmila Kulkarni-Kale Madhuri Thakar Vandana Saxena |
| author_sort | Jyotsna Gokavi |
| collection | DOAJ |
| description | TGF-β has been shown to play a differential role in either restricting or aiding HIV infection in different cell types, however its role in the cervical cells is hitherto undefined. Among females, more than 80% of infections occur through heterosexual contact where cervicovaginal mucosa plays a critical role, however the early events during the establishment of infection at female genital mucosa are poorly understood. We earlier showed that increased TGF-β level has been associated with cervical viral shedding in the HIV infected women, however a causal relationship could not be examined. Therefore, here we first established an in vitro cell-associated model of HIV infection in the cervical epithelial cells (ME-180) and demonstrated that TGF-β plays an important role as a negative regulator of HIV release in the infected cervical epithelial cells. Inhibition of miR-155 upregulated TGF-β signaling and mRNA expression of host restriction factors such as <i>APOBEC-3G</i>, <i>IFI-16</i> and <i>IFITM-3</i>, while decreased the HIV release in ME-180 cells. To conclude, this is the first study to decipher the complex interplay between TGF-β, miR-155 and HIV release in the cervical epithelial cells. Collectively, our data suggest the plausible role of TGF-β in promoting HIV latency in cervical epithelial cells which needs further investigations. |
| first_indexed | 2024-03-10T04:59:17Z |
| format | Article |
| id | doaj.art-80df93be959f469babbdb58708ec9406 |
| institution | Directory Open Access Journal |
| issn | 1999-4915 |
| language | English |
| last_indexed | 2024-03-10T04:59:17Z |
| publishDate | 2021-11-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Viruses |
| spelling | doaj.art-80df93be959f469babbdb58708ec94062023-11-23T01:57:51ZengMDPI AGViruses1999-49152021-11-011311226610.3390/v13112266Inhibition of miR-155 Promotes TGF-β Mediated Suppression of HIV Release in the Cervical Epithelial CellsJyotsna Gokavi0Sharwari Sadawarte1Anant Shelke2Urmila Kulkarni-Kale3Madhuri Thakar4Vandana Saxena5Division of Immunology and Serology, Indian Council of Medical Research-National AIDS Research Institute, MIDC, Bhosari, Pune 411026, IndiaBioinformatics Centre, Savitribai Phule Pune University, Pune 411007, IndiaBioinformatics Centre, Savitribai Phule Pune University, Pune 411007, IndiaBioinformatics Centre, Savitribai Phule Pune University, Pune 411007, IndiaDivision of Immunology and Serology, Indian Council of Medical Research-National AIDS Research Institute, MIDC, Bhosari, Pune 411026, IndiaDivision of Immunology and Serology, Indian Council of Medical Research-National AIDS Research Institute, MIDC, Bhosari, Pune 411026, IndiaTGF-β has been shown to play a differential role in either restricting or aiding HIV infection in different cell types, however its role in the cervical cells is hitherto undefined. Among females, more than 80% of infections occur through heterosexual contact where cervicovaginal mucosa plays a critical role, however the early events during the establishment of infection at female genital mucosa are poorly understood. We earlier showed that increased TGF-β level has been associated with cervical viral shedding in the HIV infected women, however a causal relationship could not be examined. Therefore, here we first established an in vitro cell-associated model of HIV infection in the cervical epithelial cells (ME-180) and demonstrated that TGF-β plays an important role as a negative regulator of HIV release in the infected cervical epithelial cells. Inhibition of miR-155 upregulated TGF-β signaling and mRNA expression of host restriction factors such as <i>APOBEC-3G</i>, <i>IFI-16</i> and <i>IFITM-3</i>, while decreased the HIV release in ME-180 cells. To conclude, this is the first study to decipher the complex interplay between TGF-β, miR-155 and HIV release in the cervical epithelial cells. Collectively, our data suggest the plausible role of TGF-β in promoting HIV latency in cervical epithelial cells which needs further investigations.https://www.mdpi.com/1999-4915/13/11/2266HIVcervicalTGF-βmicroRNAhost restriction factorsmiR-155 |
| spellingShingle | Jyotsna Gokavi Sharwari Sadawarte Anant Shelke Urmila Kulkarni-Kale Madhuri Thakar Vandana Saxena Inhibition of miR-155 Promotes TGF-β Mediated Suppression of HIV Release in the Cervical Epithelial Cells Viruses HIV cervical TGF-β microRNA host restriction factors miR-155 |
| title | Inhibition of miR-155 Promotes TGF-β Mediated Suppression of HIV Release in the Cervical Epithelial Cells |
| title_full | Inhibition of miR-155 Promotes TGF-β Mediated Suppression of HIV Release in the Cervical Epithelial Cells |
| title_fullStr | Inhibition of miR-155 Promotes TGF-β Mediated Suppression of HIV Release in the Cervical Epithelial Cells |
| title_full_unstemmed | Inhibition of miR-155 Promotes TGF-β Mediated Suppression of HIV Release in the Cervical Epithelial Cells |
| title_short | Inhibition of miR-155 Promotes TGF-β Mediated Suppression of HIV Release in the Cervical Epithelial Cells |
| title_sort | inhibition of mir 155 promotes tgf β mediated suppression of hiv release in the cervical epithelial cells |
| topic | HIV cervical TGF-β microRNA host restriction factors miR-155 |
| url | https://www.mdpi.com/1999-4915/13/11/2266 |
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