Cardiac pericytes mediate the remodeling response to myocardial infarction.

Despite the prevalence of pericytes in the microvasculature of the heart, their role during ischemia-induced remodeling remains unclear. We used multiple lineage-tracing mouse models and found that pericytes migrated to the injury site and expressed profibrotic genes, coinciding with increased vessel leakage after myocardial infarction (MI). Single-cell RNA-Seq of cardiac pericytes at various time points after MI revealed the temporally regulated induction of genes related to vascular permeability, extracellular matrix production, basement membrane degradation, and TGF-ß signaling. Deleting TGF-ß receptor 1 in chondroitin sulfate proteoglycan 4-expressing (Cspg4-expressing) cells reduced fibrosis following MI, leading to a transient improvement in the cardiac ejection fraction. Furthermore, genetic ablation of Cspg4-expressing cells resulted in excessive vascular permeability, a decline in cardiac function, and increased mortality in the second week after MI. These data reveal an essential role for cardiac pericytes in the control of vascular homeostasis and the fibrotic response after acute ischemic injury, information that will help guide the development of novel strategies to preserve vascular integrity and attenuate pathological cardiac remodeling.

Clonal Tracing of Heart Regeneration.

Cardiomyocytes in the adult mammalian heart have a low turnover during homeostasis. After myocardial injury, there is irreversible loss of cardiomyocytes, which results in subsequent scar formation and cardiac remodeling. In order to better understand and characterize the proliferative capacity of cardiomyocytes, in vivo methods have been developed to track their fate during normal development and after injury. Lineage tracing models are of particular interest due to their ability to record cell proliferation events over a long period of time, either during development or in response to a pathological event. This paper reviews two well-studied lineage-tracing, transgenic mouse models-mosaic analysis with double markers and rainbow reporter system.

Adjacent Segment Vertebral Body Bone Density Changes as Measured By Hounsfield Units After Lumbar Spine Fusion.

OBJECTIVE: We sought to evaluate Hounsfield units (HU) at the adjacent segment after single-level transforaminal lumbar interbody fusion (TLIF) with preoperative and postoperative computed tomography scans. METHODS: We performed a retrospective study on a series of patients who underwent L4-5 TLIF, from 2007 to 2017, by 3 spine surgeons at our institution. One-hundred and forty-three total patients were identified, and 41 patients with minimum 1-year follow-up met inclusion criteria. HU values were measured on preoperative and postoperative computed tomography at the adjacent L3 segment and at L1 as a control arm. Lumbar lordosis, pelvic tilt, pelvic incidence, sacral slope, and sagittal vertical axis were also collected preoperatively and postoperatively. RESULTS: Mean preoperative HU value at L3 did not differ from the postoperative value (134.11 ± 47.14 mg/cm3 vs. 141.21 ± 55.14 mg/cm3, P = 0.34). Similarly, the mean preoperative HU value at the L1 control level region of interest did not differ from the postoperative value (150.17 ± 53.91 mg/cm3 vs. 145.78 ± 58.34 mg/cm3, P = 0.634). The interrater reliability of HU measurements was satisfactory with a resulting intraclass correlation coefficient of 0.76. CONCLUSIONS: As measured by HU, we did not observe a change in bone density or other signs of adjacent segment disease at the L3 vertebral body 12 months after L4-5 TLIF. Spinopelvic parameters were not shown to be correlated with HU changes.