Navigation Links
Protein Increase Decreases Risk of Heart Failure

According to a recent research, development of heart failure can be reduced especially in those who have already experienced at attack by enhancing the levels of a protein in the heart.//

S100A1 is the protein, whose level when increased above normal, helped in protecting animal hearts from added damage after simulated heart attacks. This was revealed by the study conducted by Cardiology researchers at the Center for Translational Medicine at Jefferson Medical College of Thomas Jefferson University in Philadelphia.

In some cases, the animals' heart function hardly changed at all. At the same time, other animals with heart cells lacking the gene for the protein couldn't handle the stress of a heart blockage; they went on to develop heart failure.

The findings provide more evidence that falling levels of S100A1 are critical in the loss of heart-pumping strength after a heart attack and play an important role in the progression to heart failure. Potential therapeutic strategies, the researchers say, may focus on restoring S100A1 levels to normal. The work appears September 19, 2006, in the American Heart Association journal Circulation.

The researchers, led by Walter Koch, Ph.D., director of the Center for Translational Medicine in the Department of Medicine in Jefferson Medical College of Thomas Jefferson University in Philadelphia, examined two types of mice: transgenic mice which had extremely high levels of the gene for and the protein S100A1, and knockout mice that lacked S100A1 altogether.

S100A1, part of a larger family of proteins called S100, is primarily found at high levels in muscle, particularly the heart. Previous studies by other researchers showed that the protein was reduced by as much as 50 percent in patients with heart failure. Several years ago, Dr. Koch and his co-workers put the human gene that makes S100A1 into a mouse, and found a resulting increase in contractile strength of the heart cell. The mice hearts worked better and had stronger beats. In subsequent work, he and co-workers used gene therapy to restore S100A1 levels – and heart function – to normal in failing animal hearts.

Congestive heart failure affects nearly five million Americans, many of whom have poor long-term prognoses, despite recent therapeutic advances. In the study, the researchers caused simulated heart attacks in the two groups of animals. "At the basal level, hearts from S100A1 knockouts don't appear to be that different," says Dr. Koch, who is W.W. Smith Professor of Medicine at Jefferson Medical College. Yet, when they caused a heart attack, "the hearts basically fell apart," he says, adding, "S100A1 appears to be a critical molecule to the adaptation of the heart to stress."

Generally, mice survive heart attacks but within a few weeks go on to develop heart failure, he notes. But without S100A1, the researchers found a more rapid onset of heart failure, which includes a higher rate of heart cell death.

The scientists compared these results to the mice with increased levels of S100A1 in the heart who also had an occluded artery and a simulated heart attack. They found the opposite effects in these mice. In fact, the hearts of these mice appeared stronger than normal mice, and did not go on to develop heart failure during the next 20 days.

"It's clear that S100A1 expression goes down after a heart attack, which is consistent with what we've seen in the past in knockouts, and the transgenic mice never lose anything," Dr. Koch says.

According to Dr. Koch, while he and his co-workers will continue to pursue new strategies using gene therapy to manipulate S100A1 levels for treating heart failure, he notes that the current study also provides insights into the potential mechanisms behind the observed S100A1 effects. They have demonstrated a newly discovered link between a certain molecular signaling pathway and changes in S100A1 le vels in the heart after heart attack.

Certain cell receptors called Gq-coupled receptors, which include alpha-adrenergic and angiotensin receptors, play a role in cardiac hypertrophy and "have been implicated in being elevated in some models of heart disease," he says. "When these agents act on the heart, they stimulate pathways that lead to apoptosis and cardiac hypertrophy. It seems that they also lead to changes in S100A1 expression.

"It's clear that whenever you want to manipulate a heart molecule that doesn't have an enzymatic function, we have to use gene therapy," he notes. "We want to know as much about this as possible in case we can come up with a small molecule that can regulate its expression.

"Perhaps antagonists that act on Gq-coupled receptors, which are being used clinically for heart failure, may be part of the mechanism of action in heart failure, which is why they appear to give beneficial results. They prevent further S100A1 decreases through this mechanism."

Source-Eurekalert
GY
'"/>




Related medicine news :

1. Lean Protein Could Be Key to Obesity Drugs
2. Evidence Links Protein Damage to Neurodegenerative diseases like Parkinsons and Alzheimers
3. Unravelling the secrets of ‘Huntingtin’ Protein - towards the treatment of ‘Huntingtons’ Disase
4. Unravelling the secrets of ‘Huntingtin’ Protein - towards the treatment of Huntingtins’ Disese
5. Protein in urine foresees heart disease
6. Levels Of Blood Proteins May Help Heart Disease Care
7. Protein signals need for heart surgery
8. Protein and fat improve memory
9. Clotting Protein plays a role in nerve repair
10. High Levels of Protein Linked to Brain Shrinkage
11. Protein can change worn muscle fibres
Post Your Comments:
*Name:
*Comment:
*Email:


(Date:5/28/2016)... ... May 28, 2016 , ... May 26, 2016- In ... Arts Fighting Challenge with theme event of “K Warriors” on June 4, 2016 at ... , The event is sponsored and hosted by Shaolin Institute and sanctioned by ...
(Date:5/27/2016)... , ... May 27, 2016 , ... Two director-level employees ... YWCA Tribute to Women and Industry (TWIN) 2016 honorees. The award recognizes businesswomen ... For this year, Geri Boone, Director of the MLTSS (Managed Long-Term Services and Supports) ...
(Date:5/27/2016)... NY (PRWEB) , ... May 27, 2016 , ... ... casual readers, this installment is bolstered by inspiring human-interest stories, courtesy of awareness-driven ... tech within the industry, from leading advocates, associations and industry leaders such as ...
(Date:5/27/2016)... ... May 27, 2016 , ... ... students studying complementary medicine. Allison Outerbridge is this year’s Life University ... May 18 at the university’s Student Leadership Awards ceremony. , Outerbridge is approaching ...
(Date:5/26/2016)... ... May 26, 2016 , ... Cabot Corporation, Pfizer, ... respirators, according to court documents and SEC filings. A jury has returned ... v. American Optical Corporation, Case No. BC588866, Los Angeles County, California. The jury ...
Breaking Medicine News(10 mins):
(Date:5/27/2016)... 27, 2016 Kitov ... focused on late-stage drug development, today announced the ... of pivotal batches required for registration of KIT-302 ... This follows Kitov,s announcement in December ... met its primary efficacy endpoint. "We ...
(Date:5/26/2016)... 2016 TARE (Transarterial Radio-embolization) ... Savings and Overall Decreased Use of Hospital ... international specialist healthcare company, has today announced the ... Meeting of ISPOR (International Society for Pharmacoeconomics and ... (HCC) using yttrium-90 glass microspheres is associated with ...
(Date:5/25/2016)... HILDEN , Deutschland und GERMANTOWN, ... Zusammenarbeit mit Therawis bedient ... Entscheidungen bei Brustkrebs   QIAGEN N.V. ... QIA) gab heute bekannt, eine Lizenz- und Entwicklungsvereinbarung ... prädiktiver Assays für die Onkologie eingegangen zu sein. ...
Breaking Medicine Technology: