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Association Between Human Hair Loss and the Expression Levels of Nucleolin, Nucleophosmin, and UBTF Genes.
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Association Between Human Hair Loss and the Expression Levels of Nucleolin, Nucleophosmin, and UBTF Genes.
Genet Test Mol Biomarkers. 2016 Feb 11. [Epub ahead of print]
Association Between Human Hair Loss and the Expression Levels of Nucleolin, Nucleophosmin, and UBTF Genes.
Tasdemir S1, Eroz R2, Dogan H3, Erdem HB1, Sahin I1, Kara M4, Engin RI5, Turkez H6.
AIMS:
Nucleolar organizer regions, also known as argyrophilic nucleolar organizer regions, are associated with ribosomal genes. The main function of the nucleolus is the rapid production of ribosomal subunits, a process that must be highly regulated to provide the appropriate levels for cellular proliferation and cell growth. There are no studies in the literature addressing the expression and function of nucleolar component proteins, including nucleophosmin, nucleolin and the upstream binding transcription factor (UBTF), in human follicular hair cells.
METHODS:
Nineteen healthy males who had normal and sufficient hair follicles on the back of the head, but exhibited hair loss on the frontal/vertex portions of the head and 14 healthy males without hair loss were included in the current study. Gene expression levels were measured by relative quantitative real time polymerase chain reaction.
RESULTS:
In the individuals suffering from alopecia, the total expression levels of nucleolin, nucleophosmin, and UBTF were lower in normal sites than in hair loss sites. Strong expression level correlations were detected between: nucleophosmin and nucleolin; nucleophosmin and UBTF, and nucleolin and UBTF for both groups.
CONCLUSIONS:
There was an association between human hair loss and the expression levels of nucleolin, nucleophosmin, and UBTF genes.
Association Between Human Hair Loss and the Expression Levels of Nucleolin, Nucleophosmin, and UBTF Genes.
Tasdemir S1, Eroz R2, Dogan H3, Erdem HB1, Sahin I1, Kara M4, Engin RI5, Turkez H6.
AIMS:
Nucleolar organizer regions, also known as argyrophilic nucleolar organizer regions, are associated with ribosomal genes. The main function of the nucleolus is the rapid production of ribosomal subunits, a process that must be highly regulated to provide the appropriate levels for cellular proliferation and cell growth. There are no studies in the literature addressing the expression and function of nucleolar component proteins, including nucleophosmin, nucleolin and the upstream binding transcription factor (UBTF), in human follicular hair cells.
METHODS:
Nineteen healthy males who had normal and sufficient hair follicles on the back of the head, but exhibited hair loss on the frontal/vertex portions of the head and 14 healthy males without hair loss were included in the current study. Gene expression levels were measured by relative quantitative real time polymerase chain reaction.
RESULTS:
In the individuals suffering from alopecia, the total expression levels of nucleolin, nucleophosmin, and UBTF were lower in normal sites than in hair loss sites. Strong expression level correlations were detected between: nucleophosmin and nucleolin; nucleophosmin and UBTF, and nucleolin and UBTF for both groups.
CONCLUSIONS:
There was an association between human hair loss and the expression levels of nucleolin, nucleophosmin, and UBTF genes.
_________________
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Re: Association Between Human Hair Loss and the Expression Levels of Nucleolin, Nucleophosmin, and UBTF Genes.
How and why do these genes get upregulated in balding men?
YARO- Posts : 83
Join date : 2015-07-15
Re: Association Between Human Hair Loss and the Expression Levels of Nucleolin, Nucleophosmin, and UBTF Genes.
And what can we do about it?
shaftless- Posts : 1344
Join date : 2012-08-12
Re: Association Between Human Hair Loss and the Expression Levels of Nucleolin, Nucleophosmin, and UBTF Genes.
This involves RNA transcription and protein folding, maybe involving a-sycnulcein oligomers. A simpler way to break it down is anything that promotes slowing of the aging process (reduces mitochondrial decay) will improve this production. Mutations such as these are affected by mitochondrial DNA, which is at the heart of metabolic breakdown. More on this here:
Nature. 2004 May 27;429(6990):417-23.
Premature ageing in mice expressing defective mitochondrial DNA polymerase.
Point mutations and deletions of mitochondrial DNA (mtDNA) accumulate in a variety of tissues during ageing in humans, monkeys and rodents. These mutations are unevenly distributed and can accumulate clonally in certain cells, causing a mosaic pattern of respiratory chain deficiency in tissues such as heart, skeletal muscle and brain. In terms of the ageing process, their possible causative effects have been intensely debated because of their low abundance and purely correlative connection with ageing. We have now addressed this question experimentally by creating homozygous knock-in mice that express a proof-reading-deficient version of PolgA, the nucleus-encoded catalytic subunit of mtDNA polymerase. Here we show that the knock-in mice develop an mtDNA mutator phenotype with a threefold to fivefold increase in the levels of point mutations, as well as increased amounts of deleted mtDNA. This increase in somatic mtDNA mutations is associated with reduced lifespan and premature onset of ageing-related phenotypes such as weight loss, reduced subcutaneous fat, alopecia (hair loss), kyphosis (curvature of the spine), osteoporosis, anaemia, reduced fertility and heart enlargement. Our results thus provide a causative link between mtDNA mutations and ageing phenotypes in mammals.
Nature. 2004 May 27;429(6990):417-23.
Premature ageing in mice expressing defective mitochondrial DNA polymerase.
Point mutations and deletions of mitochondrial DNA (mtDNA) accumulate in a variety of tissues during ageing in humans, monkeys and rodents. These mutations are unevenly distributed and can accumulate clonally in certain cells, causing a mosaic pattern of respiratory chain deficiency in tissues such as heart, skeletal muscle and brain. In terms of the ageing process, their possible causative effects have been intensely debated because of their low abundance and purely correlative connection with ageing. We have now addressed this question experimentally by creating homozygous knock-in mice that express a proof-reading-deficient version of PolgA, the nucleus-encoded catalytic subunit of mtDNA polymerase. Here we show that the knock-in mice develop an mtDNA mutator phenotype with a threefold to fivefold increase in the levels of point mutations, as well as increased amounts of deleted mtDNA. This increase in somatic mtDNA mutations is associated with reduced lifespan and premature onset of ageing-related phenotypes such as weight loss, reduced subcutaneous fat, alopecia (hair loss), kyphosis (curvature of the spine), osteoporosis, anaemia, reduced fertility and heart enlargement. Our results thus provide a causative link between mtDNA mutations and ageing phenotypes in mammals.
_________________
My regimen
http://www.immortalhair.org/mpb-regimen
Now available for consultation (hair and/or health)
http://www.immortalhair.org/health-consultation
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