MicroRNA-mediated calcineurin signaling activation induces CCL2, CCL3, CCL5, IL8, and chemotactic activities in 4,4′-methylene diphenyl diisocyanate exposed macrophages
Advanced Search
Select up to three search categories and corresponding keywords using the fields to the right. Refer to the Help section for more detailed instructions.

Search our Collections & Repository

All these words:

For very narrow results

This exact word or phrase:

When looking for a specific result

Any of these words:

Best used for discovery & interchangable words

None of these words:

Recommended to be used in conjunction with other fields

Language:

Dates

Publication Date Range:

to

Document Data

Title:

Document Type:

Library

Collection:

Series:

People

Author:

Help
Clear All

Query Builder

Query box

Help
Clear All

For additional assistance using the Custom Query please check out our Help Page

i

MicroRNA-mediated calcineurin signaling activation induces CCL2, CCL3, CCL5, IL8, and chemotactic activities in 4,4′-methylene diphenyl diisocyanate exposed macrophages

Filetype[PDF-1.05 MB]


  • English
    • Details Supporting Files You May Also Like

    Details:

    • Alternative Title:
      Xenobiotica
    • Publisher's site:
    • Personal Author:
    • Description:
      Occupational exposure to 4,4'-methylene diphenyl diisocyanate (MDI), the most widely used monomeric diisocyanate, is one of the leading causes of occupational asthma (OA). Previously, we identified |-mediated PPP3CA/calcineurin signalling regulated | transcription in macrophages and bronchoalveolar lavage cells (BALCs) after acute MDI exposure; however, whether PPP3CA/calcineurin signalling participates in regulation of other asthma-associated mediators secreted by macrophages/BALCs after MDI exposure is unknown.Several asthma-associated, macrophage-secreted mediator mRNAs from MDI exposed murine BALCs and MDI-glutathione (GSH) conjugate treated differentiated THP-1 macrophages were analysed using RT-qPCR.Endogenous |, |, |, |, |, and | were upregulated in MDI or MDI-GSH conjugate exposed BALCs and macrophages, respectively. Calcineurin inhibitor tacrolimus (FK506) attenuated the MDI-GSH conjugate-mediated induction of |, |, |, and | but not others. Transfection of either miR-inhibitor-206-3p or miR-inhibitor-381-3p in macrophages induced chemokine |, |, |, and | transcription, whereas FK506 attenuated the miR-inhibitor-206-3p or miR-inhibitor-381-3p-mediated effects. Finally, MDI-GSH conjugate treated macrophages showed increased chemotactic ability to various immune cells, which may be attenuated by FK506.In conclusion, these results indicate that MDI exposure to macrophages/BALCs may recruit immune cells into the airway via induction of chemokines by | and |-mediated calcineurin signalling activation.
    • Subject:
    • Source:
      Xenobiotica. 51(12):1436-1452
    • Pubmed ID:
      34775880
    • Pubmed Central ID:
      PMC8915863
    • Document Type:
      Journal Article
    • Funding:
      CC999999/ImCDC/Intramural CDC HHSUnited States/
    • Collection(s):
    • Main Document Checksum:
    • Download URL:
    • File Type:

    You May Also Like

    Checkout today's featured content at stacks.cdc.gov