DALLAS -- Myoglobin, the protein long thought to be the solecarrier of oxygen to heart and certain skeletal muscle, is notnecessary for survival, UT Southwestern Medical Center at Dallasscientists reported in the October 29 issue of the journal Nature.
Because of this discovery, investigators will be able to delvefurther into causes, prevention and cures for heart failure. Theresearchers made their breakthrough by developing a strain ofmice lacking the gene to produce myoglobin, which transportsoxygen from capillaries to mitochondria in heart and endurancemuscle cells. Mitochondria are the structures within cells thattransform oxygen and other molecules into energy for allcellular functions.
"Myoglobin is found in the heart and the slow-twitch, orendurance, skeletal muscles in a number of species. So becauseof its prevalence and the energy required for contraction of theheart, we predicted that mice could not live without thisprotein," said Dr. Dan Garry, assistant professor of internalmedicine and first author of the report. "We were surprised thatnot only did they survive without it, they were born, developed,reproduced, nurtured and exercised normally."
The mice were exercised on treadmills along with littermatesthat had myoglobin. All the animals were exposed to conditionssimulating different altitudes at which the body would normallyexperience some lack of oxygen. Neither group showed anydifferences in their behavior or their ability to handle thedifferent conditions.
The only alteration researchers found in the rodents lackingmyoglobin was that the heart and endurance muscles werenonpigmented or almost white rather than a rich pink becausemost of the red color actually comes from the myoglobin. "Ourresearch suggests that the system transferring the oxygennecessary to fuel the contraction of heart and slow-twitchmuscles is much more complicated than the long-held paradigm,"Garry said.
Now, the researchers will look for other genes that areexpressed at a higher level in the genetically altered miceduring times when they are exposed to conditions where theirhearts and endurance muscles need more oxygen. In studying thesegenes, the investigators may be able to discover the system thatenables the heart and skeletal muscles to get the energy theyneed to continue functioning.
"We still believe that myoglobin is important, but somethingelse is also important; there are some cellular adaptations thatwe have not yet defined," Garry said. "By understanding andidentifying these adaptations, we will increase our knowledge ofwhat happens when people get chest pains. This will impact ourtreatment of patients who suffer from coronary-artery disease."
The other researchers on the study were: Dr. George Ordway,associate professor of physiology; Dr. Nina Radford, assistantprofessor of internal medicine; Dr. Eva Chin, postdoctoralfellow in internal medicine; Dr. Robert Grange, assistantinstructor of physiology; Dr. Rhonda Bassel-Duby, associateprofessor of internal medicine; Dr. R. Sanders Williams, chiefof cardiology, director of the Frank M. Ryburn Jr. Cardiaccenter and holder of the James T. Willerson, M.D., DistinguishedChair in Cardiovascular Diseases; and Dr. John Lorenz,Department of Molecular and Cellular Physiology, University ofCincinnati.
This work was supported by grants from the National Institutesof Health and the American Heart Association.
The above post is reprinted from materials provided by University Of Texas Southwestern Medical Center At Dallas. Note: Materials may be edited for content and length.
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