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Telocytes (TCs) are a controversial cell type characterized by the presence of a particular kind of prolongations, known as telopodes, which are long, thin, and moniliform. A number of attempts has been made to establish the molecular phenotype of cardiac TCs (i.e., expression of c-kit, CD34, vimentin, PDGRFα, PDGRFβ, etc.). We designed an immunohistochemical study involving cardiac tissue samples obtained from 10 cadavers with the aim of determining whether there are TC-like interstitial cells that populate the interstitial space other than the mural microvascular cells. We applied the markers for CD31, CD34, PDGRFα, CD117/c-kit, and α-smooth muscle actin (α-SMA). We found that, in relation to two-dimensional cuts, the endothelial tubes could be misidentified as TC-like cells, the difference being the positive identification of endothelial lumina. Moreover, we found that cardiac pericytes express PDGRFα, CD117/c-kit, and α-SMA, and that they could also be misidentified as TCs when using light microscopy. We reviewed the respective values of the previously identified markers for achieving a clear-cut identification of cardiac TCs, highlighting the critical lack of specificity.

Introduction Atrial fibrillation (AF) is nowadays considered to be one of the most important causes of heart failure, stroke, cognitive decline, vascular dementia, sudden death and overall cardiovascular morbidity. Recently were published a few articles suggesting a possible involvement of telocytes in the development of atrial fibrillation. The purpose of this article is to analyze the results obtained in the field systematically, and to see if there is enough data to support a possible involvement of telocytes in arrhythmogenesis. Materials and methods To this end, we performed a systematic review of the relevant scientific literature, indexed in PubMed, Web of Science, and Scopus. Results and discussions Our systematic review of the published data identified five articles containing original data, based on which the association between telocytes and atrial fibrillation was inferred in later studies. We analyzed the usefulness of the information contained in the original articles to support this association, showing a lack of definite proofs correlating telocytes with atrial fibrillation. Conclusions Even if a few articles implied a potential association between AF and telocytes, the current data is not enough to support it. Moreover, even an association between the morphology, characteristics, or density of the telocytes in the atrium/pulmonary veins and AF is potentially speculative, and more studies should be performed before implying it with a reasonable degree of certainty.

A great interest has developed over the last several years in research on interstitial Cajal-like cells (ICLCs), later renamed to telocytes (TCs). Such studies are restricted by diverse limitations. We aimed to critically review (sub)epicardial ICLCs/TCs and to bring forward supplemental immunohistochemical evidence on (sub)epicardial stromal niche inhabitants. We tested the epicardial expressions of CD117/c-kit, CD34, Cytokeratin 7 (CK7), Ki67, Platelet-Derived Growth Factor Receptor (PDGFR)-α and D2-40 in adult human cardiac samples. The mesothelial epicardial cells expressed D2-40, CK7, CD117/c-kit and PDGFR-α. Subepicardial D2-40-positive lymphatic vessels and isolated D2-40-positive and CK7-positive subepicardial cells were also found. Immediate submesothelial spindle-shaped cells expressed Ki-67. Submesothelial stromal cells and endothelial tubes were PDGFR-α-positive and CD34-positive. The expression of CD34 was pan-stromal, so a particular stromal cell type could not be distinguished. The stromal expression of CD117/c-kit was also noted. It seems that epicardial TCs could not be regarded as belonging to a unique cell type until (pre)lymphatic endothelial cells are inadequately excluded. Markers such as CD117/c-kit or CD34 seem to be improper for identifying TCs as a distinctive cell type. Care should be taken when using the immunohistochemical method and histological interpretations, as they may not produce accurate results.

The recovery of genetic information from highly degraded or minute amount of biological samples needs special approaches together with conventional STR multiplex assays. In this respect, the "mini-STR" technology is considered to be remarkable for its capacity to decrease the rate of failures and inconclusive results in forensic casework. By using miniSTRs, the PCR efficiency is significantly improved as shorter PCR amplicons are generated with STR primers located closer to the repeat regions. In this article we aimed to present several practical considerations regarding the miniSTR genotyping for challenging forensic samples. Looking for a robust protocol to re-investigate some of our cases with inconclusive or no typing results we studied the efficiency of a miniSTR approach. We report by comparison our results obtained with a commercial miniSTR multiplex assay on samples previously tested with two different 16 STR commercial kits. Our conclusion is definitely in favor of including in the routine protocol the miniSTR assay as it was able to improve the results, providing better or even complete DNA profiles for the difficult samples where the conventional STR kits failed.

The discovery of cardiac stem cells (CSCs) able to renew the pool of cardiomyocyte raised the question of how these cells can be recognized and directed towards cardiac reconstruction after severe ischemic injury. The functional studies demonstrated that the differentiation of adult cardiac stem cells reproduce the stages observed in the embryonic development. Each stage is characterized by a complex molecular signature, which can be used for identification and molecular targeting. Three major markers have been used to isolate CSCs: c-kit, Sca-1, and Isl1 and different progenitor populations have been described: side-population (SP), cardiosphere-derived, epicardial-derived. Combinations between the main three markers and other transcription factors, cell surface proteins and regulatory RNAs may delimit even further the cardiac precursors. Accumulation of data leads to the idea that a single, yet unidentified unique cardiac stem cell is at the origin of those observed variants. In this review, we intended to summarize the actual knowledge about the main molecular markers of cardiac stem cells.