Human Chorionic Stem Cells: Podocyte Differentiation and Potential for the Treatment of Alport Syndrome

Moschidou, Dafni; Corcelli, Michelangelo; Hau, Kwan-Leong; Ekwalla, Victoria J; Behmoaras, Jacques; Coppi, Paolo De; David, Anna L.; Bou‐Gharios, George; Cook, H. Terence; Pusey, Charles D.; Fisk, Nicholas M.; Guillot, Pascale V.

doi:10.1089/scd.2015.0305

Cited by 21 publications

(14 citation statements)

References 22 publications

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“…Instead, they confirm that OCT4A is not expressed in hAFSCs expanded in vitro in non-pluripotent conditions. Interestingly, we have reported that SS-hAFSCs may be more plastic than their postnatal counterparts since when they are cultivated in pluripotent conditions in the presence of valproic acid (VPA), they up-regulated OCT4A expression and reverted to functional bona fide pluripotency by reactivating the OCT4-downstream pluripotent pathway 27,31,40 . This suggests that despite OCT4A being downregulated, DNA conformation at the epigenetic level might be permissive to OCT4A reactivation.…”

Section: Discussionmentioning

confidence: 99%

Human mid-trimester amniotic fluid (stem) cells lack expression of the pluripotency marker OCT4A

Vlahova

Hawkins

Ranzoni

et al. 2019

Sci Rep

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Expression of OCT4A is one of the hallmarks of pluripotency, defined as a stem cell’s ability to differentiate into all the lineages of the three germ layers. Despite being defined as non-tumorigenic cells with high translational potential, human mid-trimester amniotic fluid stem cells (hAFSCs) are often described as sharing features with embryonic stem cells, including the expression of OCT4A, which could hinder their clinical potential. To clarify the OCT4A status of hAFSCs, we first undertook a systematic review of the literature. We then performed extensive gene and protein expression analyses to discover that neither frozen, nor fresh hAFSCs cultivated in multipotent stem cell culture conditions expressed OCT4A, and that the OCT4A positive results from the literature are likely to be attributed to the expression of pseudogenes or other OCT4 variants. To address this issue, we provide a robust protocol for the assessment of OCT4A in other stem cells.

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Section: Discussionmentioning

confidence: 99%

Human mid-trimester amniotic fluid (stem) cells lack expression of the pluripotency marker OCT4A

Vlahova

Hawkins

Ranzoni

et al. 2019

Sci Rep

Self Cite

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“…Some new drugs have entered clinical trials, such as bardoxolone methyl (Phase II/III) and RG-012 (effect on microRNA-21 interference, Phase II). Other therapies that have thus far been reported to show effects by in vivo and in vitro trials are as follows: (1) treatment with stem cells [42] and (2) treatment to control intracellular signal transduction (USAG-1) [43]. Further expected treatments are as follows: (1) nonsense read-through therapy [44] and (2) exon skipping therapy with antisense oligonucleotides or chemical compounds [45, 46].…”

Section: Treatmentmentioning

confidence: 99%

A review of clinical characteristics and genetic backgrounds in Alport syndrome

et al. 2018

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Alport syndrome (AS) is a progressive hereditary renal disease that is characterized by sensorineural hearing loss and ocular abnormalities. It is divided into three modes of inheritance, namely, X-linked Alport syndrome (XLAS), autosomal recessive AS (ARAS), and autosomal dominant AS (ADAS). XLAS is caused by pathogenic variants in COL4A5, while ADAS and ARAS are caused by those in COL4A3/COL4A4. Diagnosis is conventionally made pathologically, but recent advances in comprehensive genetic analysis have enabled genetic testing to be performed for the diagnosis of AS as first-line diagnosis. Because of these advances, substantial information about the genetics of AS has been obtained and the genetic background of this disease has been revealed, including genotype-phenotype correlations and mechanisms of onset in some male XLAS cases that lead to milder phenotypes of late-onset end-stage renal disease (ESRD). There is currently no radical therapy for AS and treatment is only performed to delay progression to ESRD using nephron-protective drugs. Angiotensin-converting enzyme inhibitors can remarkably delay the development of ESRD. Recently, some new drugs for this disease have entered clinical trials or been developed in laboratories. In this article, we review the diagnostic strategy, genotype-phenotype correlation, mechanisms of onset of milder phenotypes, and treatment of AS, among others.

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“…The experimental approaches to reduce renal damage in Alport mice included angiotensin-converting enzyme inhibition, 26 angiotensin-converting enzyme 2 or pentraxin-2 administration, 27-29 endothelin A receptor antagonism, 30 integrin-blockade, 31,32 anti-microRNA-21 oligonucleotide treatment, 33 transforming growth factor-beta antagonism, 31 uterine sensitization-associated gene-1 depletion, 34 CC chemokine receptor 1 antagonism, 35,36 lymphocyte depletion, 37 stem cell administration, [38][39][40] statin administration, 41 and manipulating podocytes to inducibly overexpress collagen a3a4a5(IV) heterotrimers. 42 The degree of protection from renal fibrosis was rather variable in these studies.…”

Section: Discussionmentioning

confidence: 99%

Identification of platelet-derived growth factor C as a mediator of both renal fibrosis and hypertension

Roeyen

Martin

Drescher

et al. 2019

Kidney International

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Human Chorionic Stem Cells: Podocyte Differentiation and Potential for the Treatment of Alport Syndrome

Cited by 21 publications

References 22 publications

Human mid-trimester amniotic fluid (stem) cells lack expression of the pluripotency marker OCT4A

Human mid-trimester amniotic fluid (stem) cells lack expression of the pluripotency marker OCT4A

A review of clinical characteristics and genetic backgrounds in Alport syndrome

Identification of platelet-derived growth factor C as a mediator of both renal fibrosis and hypertension

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