{"id":71984,"date":"2017-03-25T02:16:10","date_gmt":"2017-03-25T02:16:10","guid":{"rendered":"http:\/\/healthmedicinet.com\/news\/fainting-disorder-mechanism-figured-out\/"},"modified":"2017-03-25T02:16:10","modified_gmt":"2017-03-25T02:16:10","slug":"fainting-disorder-mechanism-figured-out","status":"publish","type":"post","link":"http:\/\/healthmedicinet.com\/news\/fainting-disorder-mechanism-figured-out\/","title":{"rendered":"Fainting disorder mechanism figured out"},"content":{"rendered":"
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\"Fainting
\n Fainting caused by POTS is regulated by switching gene function off. Credit: Imgur\/Twoisnoe
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Monash University researchers have discovered the mechanism underlying the fainting disorder, Postural Orthostatic Tachycardia Syndrome (POTS), the condition famously affecting the former lead singer of The Wiggles.\n <\/p>\n

POTS is a disorder characterised by orthostatic intolerance \u2013 having difficulty in becoming upright, particularly when standing up from a lying-down position, when a greatly reduced volume of blood returns to the heart. Symptoms can include feeling light-headed, fainting, fatigue and slurred speech. Interestingly, eighty per cent of those with the condition are women. <\/p>\n

Greg Page AM, the \u201cYellow Wiggle,\u201d left the popular children\u2019s music group in late 2006 for some years after developing symptoms associated with POTS, later dubbed \u2018Wiggles Disease\u2019. <\/p>\n

Monash Central Clinical School (CCS) investigators Professor Sam El-Osta and then PhD student Abdul Waleed Khan \u2013 who joined the CCS from the Baker Heart and Diabetes Institute with the opening of the new Department of Diabetes at Monash \u2013 have revealed that the problem has an epigenetic, rather than genetic, basis. <\/p>\n

While the gene implicated in POTS \u2013 norepinephrine transporter (NET) \u2013 was known for several decades, past research had failed to find a genetic mutation responsible for symptoms of POTS. <\/p>\n

The CCS scientists discovered chemical marks on the NET gene responsible for repressing or turning the gene off. They delved further and found that a repressor protein called MeCP2 together with a non-coding RNA (let-7i) was critical in the gene silencing.<\/p>\n

In another exciting development, the researchers, collaborating with the Baker Institute\u2019s Professor Murray Esler, demonstrated that the NET gene could be re-activated by using the FDA approved drug Vorinostat in blood cells derived from POTS study participants. <\/p>\n

\u201cThe rationale behind our research into POTS was to understand the regulatory mechanism to piece together some of the key molecules involved in NET gene reactivation,\u201d Professor El-Osta said.<\/p>\n

\u201cThe drug we used in the study targets specific molecules in the cell to restore NET gene function.\u201d<\/p>\n

POTS is a relatively rare condition but the findings may have far wider application.<\/p>\n

\u201cThis has important therapeutic implications. We have commenced clinical epigenomics studies to assess the generality of the mechanism and therapeutic potential as it pertains to essential hypertension, panic disorder and depressive illness.\u201d <\/p>\n

Professor El-Osta is now working with Professor Esler\u2019s team, which is recruiting patients for a much larger study to test the broader application of the compounds investigated, and others like it, that may also reactivate the NET gene.\n <\/p>\n

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Explore further:<\/b>
\n Poorly understood postural syndrome blights lives of young well educated women\n <\/p>\n

\n More information:<\/b>
\n Abdul Waheed Khan et al. NET silencing by let-7i in postural tachycardia syndrome, JCI Insight<\/i> (2017). DOI: 10.1172\/jci.insight.90183<\/p>\n