Solomon Ofori-Acquah
Emory University, GA·Medicine & Clinical Research
Sickle cell disease is one of the most common inherited blood disorders in the world. One of its most dangerous complications is acute chest syndrome, a sudden lung injury that often causes early death.
- Fields
Medicine & Clinical Research
Genetics
Pharmacology
- Topics
sickle cell disease
acute chest syndrome
heme
- Grants
- 1 known grant, through Jan 2027
What they work on
- Measure blood levels of HO-1, the heme-breaking enzyme, in sickle cell patients and transgenic mice, and test whether miR-494 and DNA methylation of the HMOX1 gene control it, by raising and lowering miR-494 in human blood immune cells.
- Use whole genome sequencing of sickle cell children with extremely high or low blood HO-1 levels to find genetic variants that affect the enzyme's activity independently of age, miR-494 and HMOX1 methylation.
- Test in a large cohort of sickle cell patients in Ghana whether baseline HO-1 level, miR-494, HMOX1 methylation and genome variants predict the risk of acute chest syndrome.
- Test whether HO-1 made by blood cells improves survival from acute chest syndrome, and whether a new truncated recombinant HO-1 protein rescues transgenic sickle cell mice from the syndrome.
More about the research
There is still no specific treatment for it. Children survive acute chest syndrome about ten times better than adults, and this project asks why. The answer could point to a new treatment for patients of all ages.
Why it matters
Acute chest syndrome kills many people with sickle cell disease worldwide, particularly in Africa, and no specific therapy exists. If the project shows that HO-1 explains why children fare better, a lab-made HO-1 molecule could become a treatment that works the same way for all patients. Blood markers such as HO-1 and miR-494 levels could also help doctors predict which patients face the highest risk.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Roberto Machado
University of Maryland, Baltimore, MD·Medicine & Clinical Research
Define how NAMPT, the enzyme that makes the metabolic signaling molecule NAD, controls metabolic reprogramming in pulmonary artery endothelial cells during the pulmonary hypertension response.
Kenneth Remy
Case Western Reserve University, OH·Medicine & Clinical Research
Measure how plasma proteins bind heme, the iron core of hemoglobin, during sepsis and after red blood cell transfusion compared with chronic hemolytic diseases and healthy conditions, using human patient samples.
Enrico Novelli
University of Pittsburgh, PA·Medicine & Clinical Research
Determine whether hemin, a toxic breakdown product of hemoglobin, and hypoxia (low oxygen) trigger VLA-4-driven blood-cell stickiness in sickle cell mice, measured by PET imaging with the tracer 64Cu-LLP2A.
The school
Emory University: 70 labs on PI Pages, $1.2B a year on research, 286 research doctorates a year.
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