Mouse C1qa (Complement C1q subcomponent subunit A) ELISA Kit

Objective: Extracellular vesicles secreted by cardiosphere-derived cells (CDCev) polarize macrophages toward a distinctive phenotype with enhanced phagocytic capacity (M-CDCev). These changes underlie cardioprotection by CDCev and by the parent CDCs, notably attenuating the no-reflow phenomenon following myocardial infarction, but the mechanisms are unclear. Here, we tested the hypothesis that M-CDCev are especially effective at scavenging debris from dying cells (ie, efferocytosis) to attenuate irreversible damage post-myocardial infarction. Approach and Results: In vitro efferocytosis assays with bone marrow-derived macrophages, and in vivo transgenic rodent models of myocardial infarction, demonstrate enhanced apoptotic cell clearance with M-CDCev. CDCev exposure induces sustained MerTK expression in M-CDCev through extracellular vesicle transfer of microRNA-26a (via suppression of Adam17); the cardioprotective response is lost in animals deficient in MerTK. Single-cell RNA-sequencing revealed phagocytic pathway activation in M-CDCev, with increased expression of complement factor C1qa, a phagocytosis facilitator. Conclusions: Together, these data demonstrate that extracellular vesicle modulation of MerTK and C1qa expression leads to enhanced macrophage efferocytosis and cardioprotection.

The aim of the study was to compare mRNA gene expression and serum protein levels of complement subcomponent C1qA in blood samples of Polish Holstein-Friesian cows reared in a bovine leukemia virus (BLV) seropositive herd. Using qRT-PCR and the 2-(Delta Delta Ct) method of relative quantification, we studied C1qA transcript expression in vivo in blood cells of 23 naturally BLV-infected cows, including 8 animals in subclinical persistent lymphocytosis (PL), 15 in clinically silent aleukemic state (AL) and 13 BLV non-infected controls. In comparison to the BLV uninfected animals, the C1qA transcript level was found to decrease approximately 4.7-fold and 1.75-fold in the PL and AL stages, respectively. Furthermore, the C1qA protein level in serum was examined with the competitive ELISA technique and it was found to decrease in BLV-infected animals. The average content of C1qA in serum was recorded at 31.6 +/- 3.78 mu g/ml and 54.5 +/- 5.94 mu g/ml in PL and BLV non-infected groups, respectively, with the difference found to be significant (p <= 0.05). In search of a causative DNA polymorphism within the bovine C1qA regulatory sequence, a 576bp PCR-amplified DNA fragment, containing the transcription start site and 472 bp of the proximal C1qA promoter, were sequenced. Three SNPs were identified; however, due to the low minor allele frequency their contribution to the observed C1qA gene differential expression needs to be verified in future research. We concluded that the differential expression of the complement subcomponent C1qA suggests that the bovine C1qA gene should be considered as a potential candidate gene associated with BLV resistance or pathogenesis.