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Potential of Fenugreek in Management of Kidney and Lung Disorders
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Amit D. Kandhare, Anwesha A. Mukherjee-Kandhare, Subhash L. Bodhankar
A study demonstrated the potential of dietary fenugreek seed (3%) administration against renin-angiotensin system-mediated renal damage in diabetic rats (Pradeep, Barman, and Srinivasan 2019). Fenugreek seed administration showed profound down-regulation in renal glucose transporters (GLUT-1 and GLUT-2), renal angiotensin-converting enzyme (ACE activity) and AT1 receptor expression, metabolites of the polyol pathway, and N-acetyl-β-d-glycosaminidase activity. The upregulated expression of kidney injury molecule-1, inducible nitric oxide, and type I collagen were markedly ameliorated by dietary fenugreek. Furthermore, podocyte damage was partially restored by fenugreek administration reflected by a correction in urinary nephrin, podocin, and podocalyxin markers. Diabetes-induced renal aberrations were also reduced by dietary fenugreek intake. The researcher concluded that dietary intake of fiber-rich fenugreek seeds was associated with inhibition of glucose translocation and renin-angiotensin system, which halted the development of diabetic nephropathy (Pradeep, Barman, and Srinivasan 2019).
Kidney Function and Uremia
Published in Sirshendu De, Anirban Roy, Hemodialysis Membranes, 2017
The glomerular capillaries are fenestrated with 70–90 nm diameter pores on the endothelium. The epithelial cells, or podocytes, have numerous pseudopodia. They interdigitate along the capillary walls to form slits, which are 25 nm wide, each closed by slit diaphragms.3 These slit diaphragms have surface proteins such as nephrin, podocalyxin, and P-cadherin.3 These are primarily responsible for restricting the passage of serum albumin and gamma globulins through them, maintaining their composition in the blood. Small molecules pass through the slits along with water. Thus, the basic aim served by this arrangement is to arrest the passage of any neutral solute greater than 8 nm and provide free passage to anything till 4 nm. The passage of solutes is also dependent on the charge of molecules. The total area of filtration, for humans, in the glomerular capillary is about 0.8 m2. However, this is an average estimate of the filtration area, which can be adjusted by the contraction or expansion of podocytes and, consequently, contraction of the diaphragm slits altering active filtration and affecting blood filtration rate.2
Spatial composition and turnover of the main molecules in the adult glomerular basement membrane
Published in Tissue Barriers, 2023
David W. Smith, Azin Azadi, Chang-Joon Lee, Bruce S. Gardiner
Having identified the main ECM molecules in the GBM above, we conclude this section with a brief discussion of the glycocalyx. Although glycocalyx is technically part of the cell rather than the GBM, there appears to be crucially important roles played by the molecule podocalyxin for normal GBM function.15 Podocalyxin is a sialomucin with an essential role in the formation and maintenance of podocyte foot processes.15,62 Podocalyxin is a member of the CD34 family of molecules,63 and is a long extensively O-glycosylated and sialylated, type I transmembrane protein (see Figures 1 in [62] and [63]), forming a substantial part of the sialic-acid rich, polyanionic glycocalyx. Attached to the podocyte cell surface, the glycocalyx can be seen to extend some 30 nm to 40 nm in thickness out from the cell membrane (see, for example, Figures 2 and 4 in [64]). This highly anionic glycocalyx covering the podocyte surfaces65 could function as a ‘backstop’ to the GBM, preventing large anionic ECM molecules being transported up to the slit diaphragms and then into Bowman’s space. Otherwise (if they could pass through the slit diaphragms), these large ECM molecules would be immediately lost from the GBM and/or potentially clog the slit diaphragms. Presumably the regions between the foot processes in the GBM, up to the slit diaphragms, are also completely filled with glycocalyx. This barrier must then be traversed before large molecules (e.g. ECM, albumin) can even interact with slit diaphragms.
Nestin and CD34 expression in colorectal cancer predicts improved overall survival
Published in Acta Oncologica, 2021
Athanasios Tampakis, Benjamin Weixler, Silvan Rast, Ekaterini-Christina Tampaki, Eleonora Cremonesi, Venkatesh Kancherla, Nadia Tosti, Christoph Kettelhack, Charlotte K. Y. Ng, Tarik Delko, Savas D. Soysal, Urs von Holzen, Evangelos Felekouras, Nikolaos Nikiteas, Martin Bolli, Luigi Tornillo, Luigi Terracciano, Serenella Eppenberger-Castori, Giulio C. Spagnoli, Salvatore Piscuoglio, Markus von Flüe, Silvio Däster, Raoul A. Droeser
CD34 is a transmembrane phosphoglycoprotein, primarily known as a marker of hematopoietic progenitor and stem cells [15]. Accumulating data demonstrates significant CD34 expression in different cell types, such as the multipotent mesenchymal stromal cells, interstitial dendritic cells, and epithelial progenitors [16–19]. CD34 is widely known as a marker of vascular endothelial progenitor cells [20]. Its best-described ligand is L-selectin that mediates adhesion of lymphocytes to CD34 surface proteins in the vascular endothelium [21]. In the gastrointestinal tract, CD34 expression has also been identified in the interstitial cells of Cajal (JCC) [22] in murine and human tissues [23]. Besides, it has been suggested that CD34 enables the trafficking of mast cells and eosinophils into peripheral tissues. Regarding cancer, podocalyxin, a member of the CD34 family, has been associated with malignancy and aggressive tumor profiles in embryonic carcinoma, leukemia, breast, prostate, and pancreatic cancer [16]. In various carcinomas, CD34 has been used to evaluate microvessel density and tumor neovascularization.
New therapeutic targets in chronic kidney disease progression and renal fibrosis
Published in Expert Opinion on Therapeutic Targets, 2020
Sandra Rayego-Mateos, Jose M. Valdivielso
Currently, studies in patients have tried to determine the miRNA signature in CKD. A study in urine samples from autosomal dominant polycystic kidney disease (ADPKD) patients showed that miR-1 and miR-133, miR-223/miR-199 are dysregulated compared to other CKD patients [175]. A phase I clinical trial in patients with CKD analyzed the safety of autologous peripheral-blood-derived CD34+ cell therapy. The results of this study showed that miRNAs associated to antiapoptotic response such as miR-374a-5p/miR-19a-3p/miR-106b-5p/miR-26b-5p/miR-20a-5p were reduced in CKD patients compared to healthy controls [176]. A study in 52 patients with IgA nephropathy described that some miRNAs from urinary sediments, such as miR-34a, miR-205, and miR-155, were reduced in IgA patients compared to controls and mir-21 levels were increased and associated to tubulointerstitial damage [177]. A study by Gebeshuber et al. described that miR-193a has a key role in the development of Focal segmental glomerulosclerosis (FSGS), downregulating the podocyte marker WT1 and its target genes, PODXL (podocalyxin) and NPHS1 (nephrin) [178]. Elevated levels of miR-146a were described in several human renal pathologies such as lupus nephritis [179] or IgA nephropathy [180] and in experimental models of lupus nephritis and diabetes [181,182]. In diabetic rats, miR-146a increase was related to TRAF6 and IRAK1 modulation [182]. All these results demonstrate a key role of miRNA in the origin and the progression of CKD, although more studies in patients are needed to determine whether miRNA can be used as therapeutic targets to prevent renal fibrosis.