Embryonic recall

Embryonic recall is is a hypothesis claiming that reactivation of developmental processes via gene expression in adult organisms is comparable to gene expression patterns in early embryonic growth stages.

Concept

The hypothesis of embryonic recall defines a regenerative process in the adult failing heart as analogy to the canonical pathway of the developing heart and was proposed in 2007 by Werner Mohl.[1][2] It claims that periodic coronary venous pressure elevation (PICSO) initiates embedded, but dormant developmental processes in adults during myocardial jeopardy, i.e. after myocardial infarction or heart failure. Hemodynamics in the primitive beating heart tube is sensed transducing “mechanical” epigenetic information during normal heart development into molecular signals. As known from earlier observations, Hemodynamics provides physiological feedback to cardiogenesis.[3]

That cardiogenesis is dependent on the mechanical action of blood flow was found by Miyasaka stating that heartbeat regulates cardiogenesis.[4] Peter Scambler and Lain Dykes in their discussion of Myiasaka´s paper stated[4] that the mechanical stress resulting from blood circulation can sometimes be a factor in heart development as important as more conventional mechanisms such as signalling pathways.

In analogy to cardiogenesis in the adult failing heart the embryonic recall hypothesis claims that mechanotransduction via shear stress and pulsatile stretch induced by periodic elevation of blood pressure in cardiac veins reopens this dormant developmental signal, setting regenerative impulses in the adult heart. Significant increase of Heme oxygenase 1 gene expression and vascular endothelial growth factor (VEGF) as well as production of VEGRF2 in experimental infarction underscores the resurgence of developmental stimuli by PICSO.[5]

Molecular findings correspond with risk reduction in patients with acute coronary syndromes as well as observations in heart failure patients. PICSO induced substantial risk reduction for re-infarction and Mace (major adverse cardiac events)[6] and by an upregulation of soluble factors released into the coronary circulation also in heart failure patients[7] up to 5 years endorsing the hypothesis “embryonic recall”. This clinical and preclinical experience suggest that PICSO via hemodynamic power activates regenerative processes also in adult human hearts reconnecting to pluripotent canonical pathways during cardiogenesis. The results emphasize that the proposed hypothesis “embryonic recall” claiming revival of an imbedded albeit dormant “epigenetic” process common to sculpture myocardium in the embryo, are able to redesign structure in the adult and failing heart.[2]

See also

Blastema

Further reading

Werner Mohl, Clemens Gangl, Alem Jusic ́, Thomas Aschacher, Martin De Jonge, Frank Rattay. PICSO - From Myocardial Salvage to Tissue Regeneration. Cardiovascular Revascularization Medicine. Cardiovasc Revasc Med. 2015 Jan-Feb;16(1):36-46. doi: 10.1016/j.carrev.2014.12.004

External links

Mild increase in coronary sinus pressure with coronary sinus reducer stent for treatment of refractory angina Article response Nature reviews 2009

References

  1. ↑ Mohl W, Myocardial regeneration beyond stem cell transplantation. WienKlinWochenschr2007;119:333-336.
  2. 1 2 Werner Mohl, Dejan Milasinovic, Thomas Aschacher, Alem Jusic, Abudunaibi Maimaitiaili and Frank Rattay. The Hypothesis of “Embryonic Recall”: Mechanotransduction as Common Denominator Linking Normal Cardiogenesis to Recovery in Adult Failing Hearts. J. Cardiovasc. Dev. Dis. 2014, 1(1), 73-82; doi:10.3390/jcdd1010073 Review
  3. ↑ Jones EAV. The initiation of blood flow and flow induced events in early vascular development. Seminars in Cell & Developmental Biology. 2011;22(9):1028-35
  4. 1 2 Miyasaka, K.Y.; Kida, Y.S.; Banjo, T.; Ueki, Y.; Nagayama, K.; Matsumoto, T.; Sato, M.; Ogura, T. Heartbeat regulates cardiogenesis by suppressing retinoic acid signaling via expression of miR-143. Mech. Dev. 2011, 128, 18–28. [Google Scholar] [CrossRef]
  5. ↑ Weigel G, Kajgana I, Bergmeister H, et al., Beck and back: a paradigm change in coronary sinus interventions--pulsatile stretch on intact coronary venous endothelium, J Thorac Cardiovasc Surg, 2007;133:1581-7
  6. ↑ Mohl W, Komamura K, Kasahara H, Heinze G, Glogar D, Hirayama A, Kodama K. Myocardial protection via the coronary sinus. Circ J. 2008 Apr;72(4):526-33
  7. ↑ W. Mohl, C. Khazen, T. Aschacher, et al. Soluble factors secreted into cardiac veins during PICSO enhance cardiomyocyte proliferation. Cardiovasc Res, 103 (Suppl. 1) (2014), p. S15
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