The role of cardiac tissue macrophages (cTMs) during pre- and postnatal developmental stages remains in many aspects unknown. We aimed to characterize cTM populations and their potential functions based on surface markers. Our in situ studies of immunostained cardiac tissue specimens of murine fetuses (from E11to E17) revealed that a significant number of embryonic cTMs (phenotyped by CD45, CD68, CD64, F4/80, CD11b, CD206, Lyve-1) resided mostly in the subepicardial space, not in the entire myocardial wall, as observed in adult individuals. cTMs accompanied newly developed blood and lymphatic vessels adhering to vessel walls by cellular processes. A subpopulation of CD68-positive cells was found to form accumulations in areas of massive apoptosis during the outflow tract remodeling and shortening. Flow cytometry analysis at E14 and E17 stages revealed newly defined three subpopulations:CD64low, CD64highCD206-and CD64highCD206+. The levels of mRNA expression for genes related to regulation of angiogenesis (VEGFa, VEGFb, VEGFc, bFGF), lymphangiogenesis (VEGFc) and extracellular matrix (ECM) remodeling (MMP13, Arg1, Ym1/Chil3, Retlna/FIZZ1) differed among the selected populations and/or embryonic stages. Our results demonstrate a diversity of embryonic cTMs and their tissue-specific locations, suggesting their various potential roles in regulating angiogenesis, lymphangiogenesis and ECM remodeling.

Vasculogenesis was originally defined by Risau in 1997 [Nature 386: 671-674] as the de novo formation of vessels from endothelial progenitor cells (EPCs), so-called angioblasts. Initially, this process was believed to be related only to embryonic life; however, further studies reported vasculogenesis to occur also in adult tissues. This overview presents the current knowledge about the origin, differentiation and significance of EPCs that have been observed in various diseases, tumors, and reparative processes. We also summarize the knowledge of how to activate these cells for therapeutic purposes and the outcomes of the therapies.

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Ménière’s disease is characterized by sudden episodes of vertigo accompanied by tinnitus and/or feeling of fullness in the ear as well as fluctuating sensorineural hearing loss. Despite numerous studies, the etiology of this disease remains unknown. However, the enlargement of the inner ear’s endolymphatic spaces, referred to as endolymphatic hydrops, is considered the underlying condition. Thanks to recent advances in magnetic resonance (MR) technology, it is now possible to obtain in vivo imaging of endolymphatic hydrops in patients presenting with Ménière’s disease symptoms. Visualization of the inner ear fluid compartments is achieved after gadolinium contrast is administered into the tympanic cavity or via the intravenous route. Evaluation of endolymphatic hydrops is possible as the contrast agent selectively penetrates the perilymph, and endolymph is visualized as contrast defects. The currently used radiological hydrops grading systems include qualitative, semi-quantitative, and volumetric scales. The methods are subject to ongoing modifications to increase their sensitivity and specificity. Numerous studies describe correlations between clinical symptoms and audiological and otoneurological examination results with the endolymphatic hydrops grade. MRI is also applicable in patients’ diagnostics with an incomplete or atypical course of the Ménière’s disease. In the course of the treatment, follow-up MRI scans enable assessing individual treatment modalities’ efficacy in terms of the severity of lesions and the further course of the disease within the inner ear.

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