Cardiovascular System - Heart Development - Revision history

Z8600021 at 07:35, 5 April 2020

2020-04-05T07:35:30Z

← Older revision		Revision as of 18:35, 5 April 2020
Line 31:		Line 31:
	\|-bgcolor="F5FAFF"		\|-bgcolor="F5FAFF"
	\|		\|

			* '''Review - Embryology of the Cardiac Conduction System Relevant to Arrhythmias'''{{#pmid:31400866\|PMID31400866}} "Embryogenesis of the heart involves the complex cellular differentiation of slow-conducting primary myocardium into the rapidly conducting chamber myocardium of the adult. However, small areas of relatively undifferentiated cells remain to form components of the adult cardiac conduction system (CCS) and nodal tissues. Further investigation has revealed additional areas of nodal-like tissues outside of the established CCS. The embryologic origins of these areas are similar to those of the adult CCS. Under pathologic conditions, these areas can give rise to important clinical arrhythmias."

	* '''Cardiomyocyte orientation modulated by the Numb family proteins-N-cadherin axis is essential for ventricular wall morphogenesis'''{{#pmid:31300538\|PMID31300538}} "The roles of cellular orientation during trabecular and ventricular wall morphogenesis are unknown, and so are the underlying mechanisms that regulate cellular orientation. Myocardial-specific Numb and Numblike double-knockout (MDKO) hearts display a variety of defects, including in cellular orientation, patterns of mitotic spindle orientation, trabeculation, and ventricular compaction. Furthermore, Numb- and Numblike-null cardiomyocytes exhibit cellular behaviors distinct from those of control cells during trabecular morphogenesis based on single-cell lineage tracing. We investigated how Numb regulates cellular orientation and behaviors and determined that N-cadherin levels and membrane localization are reduced in MDKO hearts. To determine how Numb regulates N-cadherin membrane localization, we generated an mCherry:Numb knockin line and found that Numb localized to diverse endocytic organelles but mainly to the recycling endosome. Consistent with this localization, cardiomyocytes in MDKO did not display defects in N-cadherin internalization but rather in postendocytic recycling to the plasma membrane. Furthermore, N-cadherin overexpression via a mosaic model partially rescued the defects in cellular orientation and trabeculation of MDKO hearts. Our study unravels a phenomenon that cardiomyocytes display spatiotemporal cellular orientation during ventricular wall morphogenesis, and its disruption leads to abnormal trabecular and ventricular wall morphogenesis."		* '''Cardiomyocyte orientation modulated by the Numb family proteins-N-cadherin axis is essential for ventricular wall morphogenesis'''{{#pmid:31300538\|PMID31300538}} "The roles of cellular orientation during trabecular and ventricular wall morphogenesis are unknown, and so are the underlying mechanisms that regulate cellular orientation. Myocardial-specific Numb and Numblike double-knockout (MDKO) hearts display a variety of defects, including in cellular orientation, patterns of mitotic spindle orientation, trabeculation, and ventricular compaction. Furthermore, Numb- and Numblike-null cardiomyocytes exhibit cellular behaviors distinct from those of control cells during trabecular morphogenesis based on single-cell lineage tracing. We investigated how Numb regulates cellular orientation and behaviors and determined that N-cadherin levels and membrane localization are reduced in MDKO hearts. To determine how Numb regulates N-cadherin membrane localization, we generated an mCherry:Numb knockin line and found that Numb localized to diverse endocytic organelles but mainly to the recycling endosome. Consistent with this localization, cardiomyocytes in MDKO did not display defects in N-cadherin internalization but rather in postendocytic recycling to the plasma membrane. Furthermore, N-cadherin overexpression via a mosaic model partially rescued the defects in cellular orientation and trabeculation of MDKO hearts. Our study unravels a phenomenon that cardiomyocytes display spatiotemporal cellular orientation during ventricular wall morphogenesis, and its disruption leads to abnormal trabecular and ventricular wall morphogenesis."

Z8600021 at 18:54, 9 December 2019

2019-12-09T18:54:54Z

← Older revision		Revision as of 05:54, 10 December 2019
Line 178:		Line 178:

	===Articles===		===Articles===
			{{#pmid:30984452}}

	{{#pmid:18295570}}		{{#pmid:18295570}}

Z8600021 at 00:23, 7 August 2019

2019-08-07T00:23:16Z

← Older revision		Revision as of 11:23, 7 August 2019
Line 32:		Line 32:
	\|		\|
	* '''Cardiomyocyte orientation modulated by the Numb family proteins-N-cadherin axis is essential for ventricular wall morphogenesis'''{{#pmid:31300538\|PMID31300538}} "The roles of cellular orientation during trabecular and ventricular wall morphogenesis are unknown, and so are the underlying mechanisms that regulate cellular orientation. Myocardial-specific Numb and Numblike double-knockout (MDKO) hearts display a variety of defects, including in cellular orientation, patterns of mitotic spindle orientation, trabeculation, and ventricular compaction. Furthermore, Numb- and Numblike-null cardiomyocytes exhibit cellular behaviors distinct from those of control cells during trabecular morphogenesis based on single-cell lineage tracing. We investigated how Numb regulates cellular orientation and behaviors and determined that N-cadherin levels and membrane localization are reduced in MDKO hearts. To determine how Numb regulates N-cadherin membrane localization, we generated an mCherry:Numb knockin line and found that Numb localized to diverse endocytic organelles but mainly to the recycling endosome. Consistent with this localization, cardiomyocytes in MDKO did not display defects in N-cadherin internalization but rather in postendocytic recycling to the plasma membrane. Furthermore, N-cadherin overexpression via a mosaic model partially rescued the defects in cellular orientation and trabeculation of MDKO hearts. Our study unravels a phenomenon that cardiomyocytes display spatiotemporal cellular orientation during ventricular wall morphogenesis, and its disruption leads to abnormal trabecular and ventricular wall morphogenesis."		* '''Cardiomyocyte orientation modulated by the Numb family proteins-N-cadherin axis is essential for ventricular wall morphogenesis'''{{#pmid:31300538\|PMID31300538}} "The roles of cellular orientation during trabecular and ventricular wall morphogenesis are unknown, and so are the underlying mechanisms that regulate cellular orientation. Myocardial-specific Numb and Numblike double-knockout (MDKO) hearts display a variety of defects, including in cellular orientation, patterns of mitotic spindle orientation, trabeculation, and ventricular compaction. Furthermore, Numb- and Numblike-null cardiomyocytes exhibit cellular behaviors distinct from those of control cells during trabecular morphogenesis based on single-cell lineage tracing. We investigated how Numb regulates cellular orientation and behaviors and determined that N-cadherin levels and membrane localization are reduced in MDKO hearts. To determine how Numb regulates N-cadherin membrane localization, we generated an mCherry:Numb knockin line and found that Numb localized to diverse endocytic organelles but mainly to the recycling endosome. Consistent with this localization, cardiomyocytes in MDKO did not display defects in N-cadherin internalization but rather in postendocytic recycling to the plasma membrane. Furthermore, N-cadherin overexpression via a mosaic model partially rescued the defects in cellular orientation and trabeculation of MDKO hearts. Our study unravels a phenomenon that cardiomyocytes display spatiotemporal cellular orientation during ventricular wall morphogenesis, and its disruption leads to abnormal trabecular and ventricular wall morphogenesis."

			* '''Myoarchitectural disarray of hypertrophic cardiomyopathy begins pre-birth'''{{#pmid:31347708\|PMID31347708}} "Myoarchitectural disarray - the multiscalar disorganisation of myocytes, is a recognised histopathological hallmark of adult human hypertrophic cardiomyopathy (HCM). It occurs before the establishment of left ventricular hypertrophy (LVH) but its early origins and evolution around the time of birth are unknown. Our aim is to investigate whether myoarchitectural abnormalities in HCM are present in the fetal heart. We used wild-type, heterozygous and homozygous hearts (n = 56) from a Mybpc3-targeted knock-out HCM mouse model and imaged the 3D micro-structure by high-resolution episcopic microscopy. We developed a novel structure tensor approach to extract, display and quantify myocyte orientation and its local angular uniformity by helical angle, angle of intrusion and myoarchitectural disarray index, respectively, immediately before and after birth. In wild-type, we demonstrate uniformity of orientation of cardiomyocytes with smooth transitions of helical angle transmurally both before and after birth but with traces of disarray at the septal insertion points of the right ventricle. In comparison, heterozygous mice free of LVH, and homozygous mice showed not only loss of the normal linear helical angulation transmural profiles observed in wild-type but also fewer circumferentially arranged myocytes at birth. Heterozygous and homozygous showed more disarray with a wider distribution than in wild-type before birth. In heterozygous mice, disarray was seen in the anterior, septal and inferior walls irrespective of stage, whereas in homozygous mice it extended to the whole LV circumference including the lateral wall."

	* '''Krox20 defines a subpopulation of cardiac neural crest cells contributing to arterial valves and bicuspid aortic valve Development'''{{#pmid:29158447\|PMID29158447}} "Although cardiac neural crest cells are required at early stages of arterial valve development, their contribution during valvular leaflet maturation remains poorly understood. Here, we show in mouse that neural crest cells from pre-otic and post-otic regions make distinct contributions to the arterial valve leaflets.... Our findings demonstrate a crucial role for Krox20 in arterial valve development and reveal that an excess of neural crest cells may be associated with bicuspid aortic valve." {{neural crest}}		* '''Krox20 defines a subpopulation of cardiac neural crest cells contributing to arterial valves and bicuspid aortic valve Development'''{{#pmid:29158447\|PMID29158447}} "Although cardiac neural crest cells are required at early stages of arterial valve development, their contribution during valvular leaflet maturation remains poorly understood. Here, we show in mouse that neural crest cells from pre-otic and post-otic regions make distinct contributions to the arterial valve leaflets.... Our findings demonstrate a crucial role for Krox20 in arterial valve development and reveal that an excess of neural crest cells may be associated with bicuspid aortic valve." {{neural crest}}

Z8600021 at 00:18, 7 August 2019

2019-08-07T00:18:58Z

@@ Line 35: / Line 35: @@
 * '''Krox20 defines a subpopulation of cardiac neural crest cells contributing to arterial valves and bicuspid aortic valve Development'''{{#pmid:29158447|PMID29158447}} "Although cardiac neural crest cells are required at early stages of arterial valve development, their contribution during valvular leaflet maturation remains poorly understood. Here, we show in mouse that neural crest cells from pre-otic and post-otic regions make distinct contributions to the arterial valve leaflets.... Our findings demonstrate a crucial role for Krox20 in arterial valve development and reveal that an excess of neural crest cells may be associated with bicuspid aortic valve." {{neural crest}}
 |}
 ==Textbooks==
 ===UNSW Embryology===

Z8600021 at 00:16, 7 August 2019

2019-08-07T00:16:45Z

← Older revision		Revision as of 11:16, 7 August 2019
Line 27:		Line 27:

	{{Heart Links}}		{{Heart Links}}

	== Some Recent Findings ==		== Some Recent Findings ==
	{\|		{\|
	\|-bgcolor="F5FAFF"		\|-bgcolor="F5FAFF"
	\|		\|
			* '''Cardiomyocyte orientation modulated by the Numb family proteins-N-cadherin axis is essential for ventricular wall morphogenesis'''{{#pmid:31300538\|PMID31300538}} "The roles of cellular orientation during trabecular and ventricular wall morphogenesis are unknown, and so are the underlying mechanisms that regulate cellular orientation. Myocardial-specific Numb and Numblike double-knockout (MDKO) hearts display a variety of defects, including in cellular orientation, patterns of mitotic spindle orientation, trabeculation, and ventricular compaction. Furthermore, Numb- and Numblike-null cardiomyocytes exhibit cellular behaviors distinct from those of control cells during trabecular morphogenesis based on single-cell lineage tracing. We investigated how Numb regulates cellular orientation and behaviors and determined that N-cadherin levels and membrane localization are reduced in MDKO hearts. To determine how Numb regulates N-cadherin membrane localization, we generated an mCherry:Numb knockin line and found that Numb localized to diverse endocytic organelles but mainly to the recycling endosome. Consistent with this localization, cardiomyocytes in MDKO did not display defects in N-cadherin internalization but rather in postendocytic recycling to the plasma membrane. Furthermore, N-cadherin overexpression via a mosaic model partially rescued the defects in cellular orientation and trabeculation of MDKO hearts. Our study unravels a phenomenon that cardiomyocytes display spatiotemporal cellular orientation during ventricular wall morphogenesis, and its disruption leads to abnormal trabecular and ventricular wall morphogenesis."

	* '''Krox20 defines a subpopulation of cardiac neural crest cells contributing to arterial valves and bicuspid aortic valve Development'''{{#pmid:29158447\|PMID29158447}} "Although cardiac neural crest cells are required at early stages of arterial valve development, their contribution during valvular leaflet maturation remains poorly understood. Here, we show in mouse that neural crest cells from pre-otic and post-otic regions make distinct contributions to the arterial valve leaflets.... Our findings demonstrate a crucial role for Krox20 in arterial valve development and reveal that an excess of neural crest cells may be associated with bicuspid aortic valve." {{neural crest}}		* '''Krox20 defines a subpopulation of cardiac neural crest cells contributing to arterial valves and bicuspid aortic valve Development'''{{#pmid:29158447\|PMID29158447}} "Although cardiac neural crest cells are required at early stages of arterial valve development, their contribution during valvular leaflet maturation remains poorly understood. Here, we show in mouse that neural crest cells from pre-otic and post-otic regions make distinct contributions to the arterial valve leaflets.... Our findings demonstrate a crucial role for Krox20 in arterial valve development and reveal that an excess of neural crest cells may be associated with bicuspid aortic valve." {{neural crest}}
	\|}		\|}

Z8600021 at 21:53, 26 November 2018

2018-11-26T21:53:08Z

← Older revision		Revision as of 08:53, 27 November 2018
Line 66:		Line 66:

	==Timeline==		==Timeline==
			[[File:Heart_Looping_Sequence_(SEMs).jpg\|600px]]
			* Cardiogenic region - in splanchnic mesenchyme of prechordal plate region
			* Week 2 pair of thin-walled tubes
			* [[Week 3]] tubes fused, truncus arteriosus outflow, heart contracting
			* [[Week 4]] heart tube continues to elongate, curving to form S shape
			* [[Week 5]] Septation starts, atrial and ventricular
			* Septation continues, atrial septa remains open, foramen ovale
			* Week 40 At {{birth}} pressure difference closes foramen ovale leaving a fossa ovalis

	{{Madrid Heart timeline table}}		{{Madrid Heart timeline table}}

			'''Link:''' {{Timeline}}
	===Comparison Human and Mouse===		===Comparison Human and Mouse===
	Table from {{Ref-Anderson2016}}		Table from {{Ref-Anderson2016}}
Line 114:		Line 122:

	{{Historic Heart}}		{{Historic Heart}}
	==~~Human Development Timecourse~~==		==Molecular==
	[[File:Human heart developmental functional networks~~.jpg\|thumb\|Human heart developmental functional networks{{#pmid:20571530\|PMID20571530]]~~		[[File:Human heart developmental functional networks.jpg\|600px]]
	~~[[File:Heart_Looping_Sequence_(SEMs)~~.jpg\|600px]]
	* Cardiogenic region - in splanchnic mesenchyme of prechordal plate region
	* Week 2 pair of thin-walled tubes
	* [[Week 3]] tubes fused, truncus arteriosus outflow, heart contracting
	* [[Week 4]] heart tube continues to elongate, curving to form S shape
	* [[Week 5]] Septation starts, atrial and ventricular
	* Septation continues, atrial septa remains open, foramen ovale
	* Week 40 At birth pressure difference closes foramen ovale leaving a fossa ovalis

	~~'''Link:'''~~ {{~~Timeline~~}}		Human heart developmental functional networks{{#pmid:20571530\|PMID20571530}}

	==Heart Layers==		==Heart Layers==

Z8600021 at 21:49, 26 November 2018

2018-11-26T21:49:02Z

← Older revision		Revision as of 08:49, 27 November 2018
Line 136:		Line 136:
	{{Heart Volume table1}}		{{Heart Volume table1}}

			{{Heart Volume table2}}

	{~~\| class="pretty table"~~
	~~\|+ '''Stroke~~ Volume~~'''~~
	\|-
	~~! Week~~
	~~! Left Stroke Volume (ml)~~
	~~! Right Stroke Volume (ml)~~
	~~! Cardiac Output L/R (ml/min)~~
	\|-
	~~\| 10~~
	~~\| 0.02~~
	~~\| 0.01~~
	~~\| 2.39 / 1.8~~
	\|-
	~~\| 18~~
	~~\| 0.32~~
	~~\| 0.30~~
	~~\| 43.46 / 46.72~~
	\|-
	~~\| 32~~
	~~\| 2.07~~
	~~\| 2.67~~
	~~\| 284.71 / 365.99~~
	\|-
	\| colspan=4\|Table data is "embryonic age" while original reference used gestational age {{GA}} (from LMP) The stroke volume (SV) can be calculated from ultrasound measurement of end diastole volume (EDV) minus end systole volume (ESV); (SV = EDV - ESV).{{#pmid:18634132\|PMID18634132}}
	\|}

Z8600021 at 21:45, 26 November 2018

2018-11-26T21:45:47Z

← Older revision		Revision as of 08:45, 27 November 2018
Line 89:		Line 89:
	* PEO - proepicardial organ		* PEO - proepicardial organ
	\|}		\|}

	~~==Development Weeks===~~

	===Week 9===		===Week 9===

Z8600021 at 21:44, 26 November 2018

2018-11-26T21:44:45Z

← Older revision		Revision as of 08:44, 27 November 2018
Line 136:		Line 136:
	== Heart Volume ==		== Heart Volume ==

	{~~\| class="pretty table"~~		{{Heart Volume table1}}
	~~\|+ '''Heart Volume'''~~
	\|-
	~~! Week~~
	! Heart Volume ~~(ml)~~
	~~! Lung Volume (ml)~~
	\|-
	~~\| 10~~
	~~\| 0.6~~
	~~\| 1.6~~
	\|-
	~~\| 18~~
	~~\| 4.3~~
	~~\| 10.9~~
	\|-
	~~\| 30~~
	~~\| 26.6~~
	~~\| 49.3~~
	\|-
	~~\| colspan=4\|Table data is "embryonic age" while original reference used gestational age {{GA}} (from LMP){{#pmid:16388511\|PMID16388511~~}}
	\|}


	{\| class="pretty table"		{\| class="pretty table"
	~~! colspan=4~~\|Stroke Volume		\|+ '''Stroke Volume'''
	\|-		\|-
	! Week		! Week

Z8600021 at 21:43, 26 November 2018

2018-11-26T21:43:33Z

← Older revision		Revision as of 08:43, 27 November 2018
Line 90:		Line 90:
	\|}		\|}

			==Development Weeks===

	==Week 9==		===Week 9===
	Images from human heart (week 9)<ref name=Licata1954>{{Ref-Licata1954}}</ref>		Images from human heart (week 9)<ref name=Licata1954>{{Ref-Licata1954}}</ref>
	<br>		<br>
Line 120:		Line 121:
	* Cardiogenic region - in splanchnic mesenchyme of prechordal plate region		* Cardiogenic region - in splanchnic mesenchyme of prechordal plate region
	* Week 2 pair of thin-walled tubes		* Week 2 pair of thin-walled tubes
	* Week 3 tubes fused, truncus arteriosus outflow, heart contracting		* [[Week 3]] tubes fused, truncus arteriosus outflow, heart contracting
	* Week 4 heart tube continues to elongate, curving to form S shape		* [[Week 4]] heart tube continues to elongate, curving to form S shape
	* Week 5 Septation starts, atrial and ventricular		* [[Week 5]] Septation starts, atrial and ventricular
	* Septation continues, atrial septa remains open, foramen ovale		* Septation continues, atrial septa remains open, foramen ovale
	* Week 40 At birth pressure difference closes foramen ovale leaving a fossa ovalis		* Week 40 At birth pressure difference closes foramen ovale leaving a fossa ovalis