The study extracted RNA from VYS, PYS, placenta, liver, and small intestine tissues from C3H/HeSlc strain mice.
[7] This study investigated the regulation of the ENTPD2 gene and the production of the NTPDase2 protein in brain cells during neuroinflammatory and neurodegenerative conditions.
When exposed to inflammatory mediators, including IL-6, IL-1β, TNFα, and IFNγ, for 8 and 24 hours, the expression of Entpd2 (the gene encoding NTPDase2) in primary astrocytes remained unaffected at both mRNA and protein levels.
These findings provide valuable insights into the regulation of NTPDase2 in neuroinflammatory conditions, specifically highlighting the lack of impact on Entpd2 expression by certain proinflammatory cytokines in primary astrocytes.
The virus binds to angiotensin-converting enzyme 2 (ACE2) on a subset of TRCs, specifically type II cells in taste buds.
Luciferin/luciferase assays performed on the circumvallate tissue of these knockout mice revealed heightened levels of extracellular ATP.
The study proposes that the elevated extracellular ATP levels in Entpd2-knockout mice may desensitize P2X receptors associated with nerve fibers, leading to a dampening of taste responses.
Initially, they utilized RT-PCR to assess the presence of NTPDase2 mRNA in pooled taste buds from fungiform and circumvallate papillae.
The PCR results indicate the presence of all three cell types in both circumvallate and fungiform taste buds of the KO mice.
In the case of animals with the usual genetic makeup (WT), there was an observed a concentrated reaction product in taste buds when ATP, not ADP, was the substance used.
Since ATP activates P2X receptors on gustatory nerve fibers, essential for neurotransmission in the taste system, the genetic deletion of ectoATPase is proposed to disrupt purinergic transmission at this critical synapse.
In parallel, the area surrounding inactive taste tissue in Entpd2-null mice exhibits heightened nanomolar ATP concentrations, indicating a connection to the desensitization of P2X3 homomers.