<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>23(23)</volume><submitter>Silva-Gomes NLD</submitter><pubmed_abstract>Ecto-nucleoside triphosphate diphosphohydrolases (NTPDases) are enzymes located on the surface of the T.&amp;amp;nbsp;cruzi plasma membrane, which hydrolyze a wide range of tri-/-diphosphate nucleosides. In this work, we used previously developed genetically modified strains of Trypanosoma&amp;amp;nbsp;cruzi (T. cruzi), hemi-knockout (KO +/-) and overexpressing (OE) the TcNTPDase-1 gene to evaluate the parasite infectivity profile in a mouse model of acute infection (n = 6 mice per group). Our results showed significantly higher parasitemia and mortality, and lower weight in animals infected with parasites OE TcNTPDase-1, as compared to the infection with the wild type (WT) parasites. On the other hand, animals infected with (KO +/-) parasites showed no mortality during the 30-day trial and mouse weight was more similar to the non-infected (NI) animals. In addition, they had low parasitemia (45.7 times lower) when compared with parasites overexpressing TcNTPDase-1 from the hemi-knockout (OE KO +/-) group. The hearts of animals infected with the OE KO +/- and OE parasites showed significantly larger regions of cardiac inflammation than those infected with the WT parasites (p &amp;lt; 0.001). Only animals infected with KO +/- did not show individual electrocardiographic changes during the period of experimentation. Together, our results expand the knowledge on the role of NTPDases in T.&amp;amp;nbsp;cruzi infectivity, reenforcing the potential of this enzyme as a chemotherapy target to treat Chagas disease (CD).</pubmed_abstract><journal>International journal of molecular sciences</journal><pagination>14661</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9736689</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Overexpression of TcNTPDase-1 Gene Increases Infectivity in Mice Infected with Trypanosoma cruzi.</pubmed_title><pmcid>PMC9736689</pmcid><pubmed_authors>Moreira C</pubmed_authors><pubmed_authors>Fragoso S</pubmed_authors><pubmed_authors>Ruivo LAS</pubmed_authors><pubmed_authors>Batista DDGJ</pubmed_authors><pubmed_authors>Oliveira GM</pubmed_authors><pubmed_authors>Soeiro MNC</pubmed_authors><pubmed_authors>Silva-Gomes NLD</pubmed_authors><pubmed_authors>Silva CFD</pubmed_authors><pubmed_authors>Meuser-Batista M</pubmed_authors><pubmed_authors>Moreira OC</pubmed_authors></additional><is_claimable>false</is_claimable><name>Overexpression of TcNTPDase-1 Gene Increases Infectivity in Mice Infected with Trypanosoma cruzi.</name><description>Ecto-nucleoside triphosphate diphosphohydrolases (NTPDases) are enzymes located on the surface of the T.&amp;amp;nbsp;cruzi plasma membrane, which hydrolyze a wide range of tri-/-diphosphate nucleosides. In this work, we used previously developed genetically modified strains of Trypanosoma&amp;amp;nbsp;cruzi (T. cruzi), hemi-knockout (KO +/-) and overexpressing (OE) the TcNTPDase-1 gene to evaluate the parasite infectivity profile in a mouse model of acute infection (n = 6 mice per group). Our results showed significantly higher parasitemia and mortality, and lower weight in animals infected with parasites OE TcNTPDase-1, as compared to the infection with the wild type (WT) parasites. On the other hand, animals infected with (KO +/-) parasites showed no mortality during the 30-day trial and mouse weight was more similar to the non-infected (NI) animals. In addition, they had low parasitemia (45.7 times lower) when compared with parasites overexpressing TcNTPDase-1 from the hemi-knockout (OE KO +/-) group. The hearts of animals infected with the OE KO +/- and OE parasites showed significantly larger regions of cardiac inflammation than those infected with the WT parasites (p &amp;lt; 0.001). Only animals infected with KO +/- did not show individual electrocardiographic changes during the period of experimentation. Together, our results expand the knowledge on the role of NTPDases in T.&amp;amp;nbsp;cruzi infectivity, reenforcing the potential of this enzyme as a chemotherapy target to treat Chagas disease (CD).</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2025-04-20T03:33:18.601Z</modification><creation>2025-04-20T03:33:18.601Z</creation></dates><accession>S-EPMC9736689</accession><cross_references><pubmed>36498985</pubmed><doi>10.3390/ijms232314661</doi></cross_references></HashMap>