<i>Memo1</i>gene expression in kidney and bone is unaffected by dietary mineral load and calciotropic hormones

Moor, Matthias B.; Bonny, Olivier

doi:10.14814/phy2.14410

Cited by 3 publications

(6 citation statements)

References 31 publications

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“…However, kidney specific deletion of MEMO1 did not recapitulate the reciprocal changes seen in serum calcium or bone defects observed in 'whole body' postnatal MEMO1 knockouts [52]. Additionally, the regulation of MEMO1 expression is not determined by mineral load, vitamin D or parathyroid hormone, in contrast to FGF23 or KLOTHO expression [48]. Further, administration of recombinant FGF23 in mice does not result in elevated serum calcium levels although having a profound impact on serum phosphate [53]-a mineral unaffected in MEMO1 mutants [15,42,52].…”

Section: Mineralization Skeletogenesis and Mineral Homeostasismentioning

confidence: 84%

Finding MEMO—Emerging Evidence for MEMO1′s Function in Development and Disease

Schotanus

Otterloo

2020

Genes

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Although conserved throughout animal kingdoms, the protein encoded by the gene Mediator of ERBB2 Driven Cell Motility 1 or MEMO1, has only recently come into focus. True to its namesake, MEMO1 first emerged from a proteomic screen of molecules bound to the ERBB2 receptor and was found to be necessary for efficient cell migration upon receptor activation. While initially placed within the context of breast cancer metastasis—a pathological state that has provided tremendous insight into MEMO1′s cellular roles—MEMO1′s function has since expanded to encompass additional cancer cell types, developmental processes during embryogenesis and homeostatic regulation of adult organ systems. Owing to MEMO1′s deep conservation, a variety of model organisms have been amenable to uncovering biological facets of this multipurpose protein; facets ranging from the cellular (e.g., receptor signaling, cytoskeletal regulation, redox flux) to the organismal (e.g., mineralization and mineral homeostasis, neuro/gliogenesis, vasculogenesis) level. Although these facets emerge at the intersection of numerous biological and human disease processes, how and if they are interconnected remains to be resolved. Here, we review our current understanding of this ‘enigmatic’ molecule, its role in development and disease and open questions emerging from these previous studies.

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Section: Mineralization Skeletogenesis and Mineral Homeostasismentioning

confidence: 84%

Finding MEMO—Emerging Evidence for MEMO1′s Function in Development and Disease

Schotanus

Otterloo

2020

Genes

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“…We did not observe any change in Ecrg4 renal expression after short term exposure to the two hormones. This might be due to the relative short stimulation time (2h for PTH and 6h for 1,25(OH) 2 -vitamin D), even if Cyp24a1 and Cyp27b1 transcript expression, used as controls, showed substantial increase after exposure to either of these hormones [ 9 ]. As previously noted, long-term exposure to the vitamin D analog, DHTS, induced a strong Ecrg4 upregulation.…”

Section: Discussionmentioning

confidence: 99%

“…RNA from kidneys of mice injected with 1,25(OH) 2 -vitamin D and PTH as previously described [ 9 ], was used to assess the Ecrg4 expression. Tissues were homogenized in TRIzol ® Reagent solution (#15596026 Thermo Fisher, Waltham, USA) followed by extraction with 1-bromo-3-chloropropane reagent (BCP, Molecular Research Center, Cincinnati, USA) and isopropanol precipitation.…”

Section: Methodsmentioning

confidence: 99%

“…Treatments with 1,25(OH)2-vitamin D or PTH were previously reported in [ 9 ]. In brief, male C57BL/6N mice aged 13 to 15 weeks received a subcutaneous injection of 2 μg/kg body weight 1,25(OH) 2 ‐vitamin D 3 (#D1530, Sigma Aldrich, St. Louis, USA), dissolved in ethanol 1% and 99% of NaCl 0.9%.…”

Section: Methodsmentioning

confidence: 99%

“…For the analysis of organs from PTH-treated animals, material harvested from a previous study was used [ 9 ]. In this study, male 12–13 weeks old C57BL/6N mice received a subcutaneous injection of 80 μg/kg body weight human PTH 1–34 (#P3796, Sigma Aldrich, St. Louis, USA) dissolved in NaCl 0.9% or NaCl 0.9% alone as vehicle.…”

Section: Methodsmentioning

confidence: 99%

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Loss of Ecrg4 improves calcium oxalate nephropathy

Cabuzu

Ramakrishnan²,

Moor³

et al. 2022

PLoS ONE

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Kidney stone is one of the most frequent urinary tract diseases, affecting 10% of the population and displaying a high recurrence rate. Kidney stones are the result of salt supersaturation, including calcium and oxalate. We have previously identified Esophageal cancer-related gene 4 (Ecrg4) as being modulated by hypercalciuria. Ecrg4 was initially described as a tumor suppressor gene in the esophagus. Lately, it was shown to be involved as well in apoptosis, cell senescence, cell migration, inflammation and cell responsiveness to chemotherapy. To the best of our knowledge, nothing is known about ECRG4’s function in the renal tissue and its relationship with calciuria. We hypothesized that the increased expression of Ecrg4 mRNA is triggered by hypercalciuria and might modulate intratubular calcium-oxalate precipitation. In this study, we have first (i) validated the increased Ecrg4 mRNA in several types of hypercalciuric mouse models, then (ii) described the Ecrg4 mRNA expression along the nephron and (iii) assessed ECRG4’s putative role in calcium oxalate nephropathy. For this, Ecrg4 KO mice were challenged with a kidney stone-inducing diet, rich in calcium and oxalate precursor. Taken together, our study demonstrates that Ecrg4’s expression is restricted mainly to the distal part of the nephron and that the Ecrg4 KO mice develop less signs of tubular obstruction and less calcium-oxalate deposits. This promotes Ecrg4 as a modulator of renal crystallization and may open the way to new therapeutic possibilities against calcium oxalate nephropathy.

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FGFR regulator Memo1 is dispensable for FGF23 expression by osteoblasts during folic acid‐driven kidney injury

Bartos

Moor

2023

Physiological Reports

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Loss of the mediator Of cell motility 1 ( Memo1 ) in mice caused kidney disease and a bone disease with diminished osteoblast and osteoclast biomarkers in serum, resembling alterations occurring in adynamic bone disease in humans with chronic kidney disease or in Klotho‐deficient mice. Here, we investigated whether Memo1 expression in osteoblasts is required for normal bone structure and FGF23 expression. We deleted Memo1 in the osteoblast–osteocyte lineage in Memo fl/fl mice using a Cre under Col1a1 promotor to obtain osteoblast‐specific knockout (obKO) mice. We studied organs by micro‐computed tomography, qPCR, and western blot. We challenged mice with folic acid for acute kidney injury (AKI) and analyzed organs. Memo obKO were viable without changes in gross anatomy, serum electrolytes, or circulating FGF23 concentrations compared to controls. Memo1 expression was blunted in bones of Memo obKO, whereas it remained unchanged in other organs. Micro‐CT revealed no differences between genotypes in bone structure of vertebrae, femur, and tibia. During AKI, Fgf23 expression in calvaria, and renal transcriptional changes were comparable between genotypes. However, renal injury marker expression, circulating FGF23, and parathyroid hormone revealed a sex difference with more severely affected females than males of either genotype. The present data imply that Memo1 in osteoblasts is dispensable for bone structure and expression of Fgf23 . Moreover, we found evidence of potential sex differences in murine folic acid nephropathy similar to other experimental models of renal injury that are important to consider when using this experimental model of renal injury.

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Memo1gene expression in kidney and bone is unaffected by dietary mineral load and calciotropic hormones

Cited by 3 publications

References 31 publications

Finding MEMO—Emerging Evidence for MEMO1′s Function in Development and Disease

Finding MEMO—Emerging Evidence for MEMO1′s Function in Development and Disease

Loss of Ecrg4 improves calcium oxalate nephropathy

FGFR regulator Memo1 is dispensable for FGF23 expression by osteoblasts during folic acid‐driven kidney injury

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