Project description:The gene expression signature of the human kidney interstitium is not fully understood. Transcript expression of laser microdissected cortical interstitium (excluding tubules, glomeruli and large vessels) in 9 human reference nephrectomies was compared to 6 human diabetic kidney biopsy specimens. This transcriptomic data revealed novel interstitial markers and enrichment of relevant pathways. Analysis of diabetic interstitium uncovered genes with unchanged as well as down-regulated expression when compared to reference samples. Laser microdissection (LMD) methodology enables collection of transcriptomic data associated with renal interstitium to aid in interpretation of pathophysiology and precision medicine studies.
Project description:The pathogenesis and molecular signature of human acute kidney injury (AKI) remain incompletely understood, in part, owing to the heterogeneity of the disease. Further, the link between animal models and human AKI is not well characterized. Transcript expression of AKI in 39 native human renal biopsy samples was compared to 9 reference nephrectomies. These data demonstrate that the molecular signature segregates patients with AKI in spite of similar pathological and clinical phenotyping. Such molecular characterization will offer advantages in categorizing and understanding the underlying pathogenesis of phenotypically complex and heterogeneous forms of AKI.
Project description:A microarray analysis with renal biopsy specimens from CKD patients was conducted in order to identify the responsible genes associated with tubulointerstitial fibrosis and tubular cell injury in CKD. This study showed microarray profiles in total 53 biopsy specimens of CKD patients. In the discovery set, 554 down-regulated and 226 up-regulated signatures were identified. Then, the expressional changes of these genes were examined in the validation set. Gene expression profiles in human chronic kidney disease was explored using renal biopsy specimens. Two independent studies: discovery set and validation set were performed. This dataset is part of the TransQST collection.
Project description:The number of heart failure (HF) patients is increasing. HF is frequently accompanied by kidney dysfunction and such organ failure is closely related. Recent investigations revealed that increased renal venous pressure, rather than decreased cardiac output, causes the deterioration of kidney function in HF patients; however, the underlying responsible mechanisms are unknown. We demonstrated that reduced blood flow speed in peritubular capillaries (PTCs) by renal congestion and upregulation of nuclear factor-κB (NF-κB) signaling synergistically exacerbate kidney injury. We generated a novel mouse model with unilateral renal congestion by coarctation of the inferior vena cava between renal veins. Intravital imaging highlighted the notable dilatation of PTCs and decreased renal blood flow speed in the congestive kidney. Renal damage after ischemia reperfusion injury was exacerbated in the congestive kidney and accumulation of polymorphonuclear leukocytes (PMNs) within PTCs was observed at the acute phase after injury. Pharmacological inhibition of NF-κB ameliorated renal congestion-mediated exacerbation of kidney injury. In vitro, adhesion of PMNs on the TNFα-stimulated endothelial cells was accelerated by perfusion of PMNs at a slower speed, which was cancelled by the inhibition of NF-κB signaling. Our study demonstrates the importance of slower blood flow accompanying activated NF-κB signaling in the congestive kidney in the exacerbation of renal injury. These mechanisms may explain how increased renal venous pressure in HF patients causes the deterioration of kidney dysfunction. Inhibition of NF-κB signaling may be a therapeutic candidate for the vicious cycle between heart and kidney failure with increased renal venous pressure.
Project description:A microarray analysis with renal biopsy specimens from CKD patients was conducted in order to identify the responsible genes associated with tubulointerstitial fibrosis and tubular cell injury in CKD. This study showed microarray profiles in total 53 biopsy specimens of CKD patients. In the discovery set, 554 down-regulated and 226 up-regulated signatures were identified. Then, the expressional changes of these genes were examined in the validation set.
Project description:The entire small intestine was obseved by balloon endoscopy. Biopsy specimens were taken from jejunum, ileum and colon, respectively.
Project description:Skin biopsy specimens of skin lesions were profiled for miRNA expression. In this study, we indentified miRNA species that were differentially expressed in the skin lesions of either the lepromatous or tuberculoid forms of leprosy. One miRNA species, hsa-mir-21, found in the lepromatous lesions was capable of downregulating the vitamin D-dependent antimicrobial pathway. Scalpel or punch skin biopsy specimens were obtained after informed consent from patients with tuberculoid leprosy and patients with lepromatous leprosy at the time of diagnosis. Specimens were embedded in OCT medium, snap-frozen in liquid nitrogen and stored at 80°C until sectioning.
Project description:Skin biopsy specimens of skin lesions were profiled for miRNA expression. In this study, we indentified miRNA species that were differentially expressed in the skin lesions of either the lepromatous or tuberculoid forms of leprosy. One miRNA species, hsa-mir-21, found in the lepromatous lesions was capable of downregulating the vitamin D-dependent antimicrobial pathway.
Project description:Acute Kidney Injury (AKI) is a rapid renal function decline associated with pronounced morbidity and mortality. Single Cell RNA Sequencing is a powerful tool allowing for examining transcriptional changes in multiple renal cell populations involved in the injury response. Our study reveals renal developmental gene re-activation and lineage infidelity in response to ischemia/reperfusion induced AKI, along with the novel genes which might serve as markers of acute kidney disease