2017 Group Project 3 - Revision history

Z8600021: Protected "2017 Group Project 3" ([Edit=Allow only administrators] (indefinite) [Move=Allow only administrators] (indefinite))

2017-10-26T22:16:16Z

Protected "2017 Group Project 3" ([Edit=Allow only administrators] (indefinite) [Move=Allow only administrators] (indefinite))

← Older revision	Revision as of 08:16, 27 October 2017
(No difference)

Z5059996: /* Heart */

2017-10-26T09:59:49Z

Heart

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	<!-- Do not remove template above from the project page -->		<!-- Do not remove template above from the project page -->

	=~~'''~~Heart~~'''~~=		=Heart=

	==Introduction==		==Introduction==

Z5076466: /* Developmental Signalling Processes */

2017-10-26T05:24:17Z

Developmental Signalling Processes

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	===Wnt signalling===		===Wnt signalling===

	According to the primary mode of action, Wnt signalling pathways have been divided into two major classes, canonical and non-canonical Wnt signalling pathways. Both of the pathways have a role in different stages of cardiac development which could be overlapping or independent of each other. The canonical Wnt signalling pathway involves β-catenin and is activated by a number of ligands such as Wnt-1, Wnt-2, Wnt-3A, Wnt-8A, Wnt-8B, Wnt-8C, Wnt-10A, and Wnt-10B. However, the non-canonical signalling pathway is associated with planar cell polarity and Wnt/Ca2+ pathways that are activated by different ligands such as Wnt4, Wnt5A, Wnt5B, Wnt6, Wnt7A, Wnt7B, and Wnt11 <ref><pubmed>25813860</pubmed></ref>.		According to the primary mode of action, Wnt signalling pathways have been divided into two major classes, canonical and non-canonical Wnt signalling pathways. Both of the pathways have a role in different stages of cardiac development which could be overlapping or independent of each other. The canonical Wnt signalling pathway involves β-catenin and is activated by a number of ligands such as Wnt-1, Wnt-2, Wnt-3A, Wnt-8A, Wnt-8B, Wnt-8C, Wnt-10A, and Wnt-10B. However, the non-canonical signalling pathway is associated with planar cell polarity and Wnt/Ca2+ pathways that are activated by different ligands such as Wnt4, Wnt5A, Wnt5B, Wnt6, Wnt7A, Wnt7B, and Wnt11 <ref><pubmed>25813860</pubmed></ref>.

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	[[File:Wnt signalling pathways.png\|500px\|\|thumb\|none\|'''Figure 10: ''' Wnt signalling pathways - Student Image]]		[[File:Wnt signalling pathways.png\|500px\|\|thumb\|none\|'''Figure 10: ''' Wnt signalling pathways - Student Image]]


	===FGF signalling===		===FGF signalling===
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	[[File:Regulation of Nodal-Activin signalling during heart formation.png\|500px\|\|thumb\|none\|'''Figure 11: ''' Regulation of Nodal-Activin signalling during heart formation]]		[[File:Regulation of Nodal-Activin signalling during heart formation.png\|500px\|\|thumb\|none\|'''Figure 11: ''' Regulation of Nodal-Activin signalling during heart formation]]


	===The Notch pathway===		===The Notch pathway===
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	Embryo obtains vitamin A from maternal delivery of retinol via transplacental transfer. This transfer of Vitamin A is essential for fetal growth and development and any deficiency can lead to severe congenital defects. In fact, the high prevalence of heart malformation in developing countries can be partly explained by vitamin A insufficiency. Conversely, elevated levels of vitamin A during pregnancy have a toxic effect on organogenesis including heart development. Treatment with RA in rodents was one of the earliest teratogenic models of heart defects <ref name="PMID28007475"/>.		Embryo obtains vitamin A from maternal delivery of retinol via transplacental transfer. This transfer of Vitamin A is essential for fetal growth and development and any deficiency can lead to severe congenital defects. In fact, the high prevalence of heart malformation in developing countries can be partly explained by vitamin A insufficiency. Conversely, elevated levels of vitamin A during pregnancy have a toxic effect on organogenesis including heart development. Treatment with RA in rodents was one of the earliest teratogenic models of heart defects <ref name="PMID28007475"/>.


	===Sonic Hedgehog===		===Sonic Hedgehog===


	The Sonic Hedgehog (Shh) signaling pathway is one of the major trafficking networks that is responsible for regulating the key events involved in the developmental processes. The regulatory action of Shh signaling pathway is linked to the secretion, uptake and translocation of ‘Shh protein’ an important Hedgehog ligand precursor. Activation of Shh signal requires the binding of Shh to the Ptc mediate Smoothened (Smo) (Ptc-smo) receptor complex as well as induction of downstream signaling cascade <ref><pubmed>25206052</pubmed></ref>.		The Sonic Hedgehog (Shh) signaling pathway is one of the major trafficking networks that is responsible for regulating the key events involved in the developmental processes. The regulatory action of Shh signaling pathway is linked to the secretion, uptake and translocation of ‘Shh protein’ an important Hedgehog ligand precursor. Activation of Shh signal requires the binding of Shh to the Ptc mediate Smoothened (Smo) (Ptc-smo) receptor complex as well as induction of downstream signaling cascade <ref><pubmed>25206052</pubmed></ref>.

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	[[File:The Sonic Hedghehog (Shh) signalling pathway.png\|400px\|thumb\|none\|'''Figure 13:''' Sonic Hedghehog (Shh) signalling pathway]]		[[File:The Sonic Hedghehog (Shh) signalling pathway.png\|400px\|thumb\|none\|'''Figure 13:''' Sonic Hedghehog (Shh) signalling pathway]]



	==Current Research And Findings==		==Current Research And Findings==

Z5076466: /* Retinoic Acid */

2017-10-26T05:18:58Z

Retinoic Acid

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	===Retinoic Acid===		===Retinoic Acid===
	[[File:Retinoic Acid activation pathway.png\|400px\|thumb\|right\|'''Figure 12:''' Retinoic Acid activation pathway - Student Image]]		[[File:Retinoic Acid activation pathway.png\|400px\|thumb\|right\|'''Figure 12:''' Retinoic Acid activation pathway - Student Image]]
	Retinoic acid (RA), a derivative of vitamin A, has been shown to play an important role in vertebrate embryogenesis especially heart formation. RA mediates its action by binding to two families of nuclear receptors, that is the RA and the retinoid receptors (RARs and RXRs). This binding allows RA to directly regulate gene transcription. The expression of at least one of the receptor types by almost all embryonic tissues gives these tissues responsiveness to RA. Signaling of RA is regulated by enzyme that either produce or inactivate retinoids (Fig. 12) <ref ~~name="PMID25813860"~~/>		Retinoic acid (RA), a derivative of vitamin A, has been shown to play an important role in vertebrate embryogenesis especially heart formation. RA mediates its action by binding to two families of nuclear receptors, that is the RA and the retinoid receptors (RARs and RXRs). This binding allows RA to directly regulate gene transcription. The expression of at least one of the receptor types by almost all embryonic tissues gives these tissues responsiveness to RA. Signaling of RA is regulated by enzyme that either produce or inactivate retinoids (Fig. 12) <ref><pubmed>25813860</pubmed></ref>.

	At early stages, RA signaling is suggested to regulate progenitor size in that increasing RA concentrations leads to reduced heart populations in chicken and zebrafish embryos, whereas micromolecular concentrations lead to no heart formation. This regulation is though to happen by RA’s direct action on Hox gene family members such as Hoxa1 transcription factor. These transcription factors have enhancer containing RA response element (RARE). Thus, a reduction or an increase in RA signaling affects the contribution of Hoxa1-; Hoxa3- and Hoxb1-expressing progenitor cells to the heart<ref name="PMID28007475><pubmed>28007475</pubmed></ref>. At later stages of heart development, RA is involved in establishing the second heart field which forms atrial cells. Also, RA contributes to the proliferation of ventricular cells. In addition, RA has the potential to stimulate cellular differentiation of atrial and ventricular myocytes from human embryonic stem cells (hESCs). This capacity of RA has been exploited in regenerative medicine to promote atrial specification <ref><pubmed>25700171</pubmed></ref>.		At early stages, RA signaling is suggested to regulate progenitor size in that increasing RA concentrations leads to reduced heart populations in chicken and zebrafish embryos, whereas micromolecular concentrations lead to no heart formation. This regulation is though to happen by RA’s direct action on Hox gene family members such as Hoxa1 transcription factor. These transcription factors have enhancer containing RA response element (RARE). Thus, a reduction or an increase in RA signaling affects the contribution of Hoxa1-; Hoxa3- and Hoxb1-expressing progenitor cells to the heart<ref name="PMID28007475><pubmed>28007475</pubmed></ref>. At later stages of heart development, RA is involved in establishing the second heart field which forms atrial cells. Also, RA contributes to the proliferation of ventricular cells. In addition, RA has the potential to stimulate cellular differentiation of atrial and ventricular myocytes from human embryonic stem cells (hESCs). This capacity of RA has been exploited in regenerative medicine to promote atrial specification <ref><pubmed>25700171</pubmed></ref>.

Z5076466: /* Transforming growth factor-β */

2017-10-26T05:02:54Z

Transforming growth factor-β

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	===Transforming growth factor-β===		===Transforming growth factor-β===
	Transforming growth factor-β superfamily involves a large number of growth factors that are structurally related. These growth factors, including Nodal or its mimic Activin, bone morphogenic protein (BMP) and growth and differentiation factors, signal through SMAD-dependent and SMAD-independent pathways <ref><pubmed>18290874</pubmed></ref>. SMAD-dependent pathway involves the activation of SMAD proteins upon TGF-β binding to its receptor followed by SMAD transfer into the nucleus regulating gene transcription <ref><pubmed>14534577</pubmed></ref>.		Transforming growth factor-β superfamily involves a large number of growth factors that are structurally related. These growth factors, including Nodal or its mimic Activin, bone morphogenic protein (BMP) and growth and differentiation factors, signal through SMAD-dependent and SMAD-independent pathways <ref><pubmed>18290874</pubmed></ref>. SMAD-dependent pathway involves the activation of SMAD proteins upon TGF-β binding to its receptor followed by SMAD transfer into the nucleus regulating gene transcription <ref><pubmed>14534577</pubmed></ref>.
	Nodal and its mimic Activin act through SMAD-2 and -3 to activate transcription. During embryo development, epiblast cells produce high levels of Nodal growth factors leading to a gradient of nodal in these cells. This gradient is important for mesoderm patterning (left-right asymmetric heart development) and lineage specification. For this reason, this gradient is maintained by Nodal antagonist secreted from the anterior visceral endoderm or by BMP-4 and Wnt-3 feedback loop in the extraembryonic tissues (Fig.11) <ref ~~name="PMID25813860~~><pubmed>25813860</pubmed></ref>		Nodal and its mimic Activin act through SMAD-2 and -3 to activate transcription. During embryo development, epiblast cells produce high levels of Nodal growth factors leading to a gradient of nodal in these cells. This gradient is important for mesoderm patterning (left-right asymmetric heart development) and lineage specification. For this reason, this gradient is maintained by Nodal antagonist secreted from the anterior visceral endoderm or by BMP-4 and Wnt-3 feedback loop in the extraembryonic tissues (Fig.11) <ref><pubmed>25813860</pubmed></ref>
	Nodal/Activin’s important role in heart formation is demonstrated by animal models. Presence of Activin in amphibian embryo lead to activation of heart formation whereas the absence of Nodal co-receptor ,called Cripto, in mouse embryo resulted in failure of ES cells differentiation into cardiomyocytes <ref><pubmed>20830688</pubmed></ref>. Also, knocking out copies of SMAD-2 alone or both SMAD-2 ND -3 result in inappropriate specification of axial mesoderm <ref><pubmed>12842913</pubmed></ref>.		Nodal/Activin’s important role in heart formation is demonstrated by animal models. Presence of Activin in amphibian embryo lead to activation of heart formation whereas the absence of Nodal co-receptor ,called Cripto, in mouse embryo resulted in failure of ES cells differentiation into cardiomyocytes <ref><pubmed>20830688</pubmed></ref>. Also, knocking out copies of SMAD-2 alone or both SMAD-2 ND -3 result in inappropriate specification of axial mesoderm <ref><pubmed>12842913</pubmed></ref>.

Z5076466: /* Transforming growth factor-β */

2017-10-26T04:59:44Z

Transforming growth factor-β

← Older revision		Revision as of 14:59, 26 October 2017
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	===Transforming growth factor-β===		===Transforming growth factor-β===
	Transforming growth factor-β superfamily involves a large number of growth factors that are structurally related. These growth factors, including Nodal or its mimic Activin, bone morphogenic protein (BMP) and growth and differentiation factors, signal through SMAD-dependent and SMAD-independent pathways <ref><pubmed>18290874</pubmed></ref>. SMAD-dependent pathway involves the activation of SMAD proteins upon TGF-β binding to its receptor followed by SMAD transfer into the nucleus regulating gene transcription <pubmed>14534577</pubmed></ref>.		Transforming growth factor-β superfamily involves a large number of growth factors that are structurally related. These growth factors, including Nodal or its mimic Activin, bone morphogenic protein (BMP) and growth and differentiation factors, signal through SMAD-dependent and SMAD-independent pathways <ref><pubmed>18290874</pubmed></ref>. SMAD-dependent pathway involves the activation of SMAD proteins upon TGF-β binding to its receptor followed by SMAD transfer into the nucleus regulating gene transcription <ref><pubmed>14534577</pubmed></ref>.
	Nodal and its mimic Activin act through SMAD-2 and -3 to activate transcription. During embryo development, epiblast cells produce high levels of Nodal growth factors leading to a gradient of nodal in these cells. This gradient is important for mesoderm patterning (left-right asymmetric heart development) and lineage specification. For this reason, this gradient is maintained by Nodal antagonist secreted from the anterior visceral endoderm or by BMP-4 and Wnt-3 feedback loop in the extraembryonic tissues (Fig.11) <ref name="PMID25813860><pubmed>25813860</pubmed></ref>		Nodal and its mimic Activin act through SMAD-2 and -3 to activate transcription. During embryo development, epiblast cells produce high levels of Nodal growth factors leading to a gradient of nodal in these cells. This gradient is important for mesoderm patterning (left-right asymmetric heart development) and lineage specification. For this reason, this gradient is maintained by Nodal antagonist secreted from the anterior visceral endoderm or by BMP-4 and Wnt-3 feedback loop in the extraembryonic tissues (Fig.11) <ref name="PMID25813860><pubmed>25813860</pubmed></ref>
	Nodal/Activin’s important role in heart formation is demonstrated by animal models. Presence of Activin in amphibian embryo lead to activation of heart formation whereas the absence of Nodal co-receptor ,called Cripto, in mouse embryo resulted in failure of ES cells differentiation into cardiomyocytes <ref><pubmed>20830688</pubmed></ref>. Also, knocking out copies of SMAD-2 alone or both SMAD-2 ND -3 result in inappropriate specification of axial mesoderm <ref><pubmed>12842913</pubmed></ref>.		Nodal/Activin’s important role in heart formation is demonstrated by animal models. Presence of Activin in amphibian embryo lead to activation of heart formation whereas the absence of Nodal co-receptor ,called Cripto, in mouse embryo resulted in failure of ES cells differentiation into cardiomyocytes <ref><pubmed>20830688</pubmed></ref>. Also, knocking out copies of SMAD-2 alone or both SMAD-2 ND -3 result in inappropriate specification of axial mesoderm <ref><pubmed>12842913</pubmed></ref>.

Z5076466: /* Transforming growth factor-β */

2017-10-26T04:56:39Z

Transforming growth factor-β

← Older revision		Revision as of 14:56, 26 October 2017
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	===Transforming growth factor-β===		===Transforming growth factor-β===
	Transforming growth factor-β superfamily involves a large number of growth factors that are structurally related. These growth factors, including Nodal or its mimic Activin, bone morphogenic protein (BMP) and growth and differentiation factors, signal through SMAD-dependent and SMAD-independent pathways <ref><pubmed>18290874</pubmed></ref>.		Transforming growth factor-β superfamily involves a large number of growth factors that are structurally related. These growth factors, including Nodal or its mimic Activin, bone morphogenic protein (BMP) and growth and differentiation factors, signal through SMAD-dependent and SMAD-independent pathways <ref><pubmed>18290874</pubmed></ref>. SMAD-dependent pathway involves the activation of SMAD proteins upon TGF-β binding to its receptor followed by SMAD transfer into the nucleus regulating gene transcription <pubmed>14534577</pubmed></ref>.
	Nodal and its mimic Activin act through SMAD-2 and -3 to activate transcription. During embryo development, epiblast cells produce high levels of Nodal growth factors leading to a gradient of nodal in these cells. This gradient is important for mesoderm patterning (left-right asymmetric heart development) and lineage specification. For this reason, this gradient is maintained by Nodal antagonist secreted from the anterior visceral endoderm or by BMP-4 and Wnt-3 feedback loop in the extraembryonic tissues (Fig.11) <ref name="PMID25813860><pubmed>25813860</pubmed></ref>		Nodal and its mimic Activin act through SMAD-2 and -3 to activate transcription. During embryo development, epiblast cells produce high levels of Nodal growth factors leading to a gradient of nodal in these cells. This gradient is important for mesoderm patterning (left-right asymmetric heart development) and lineage specification. For this reason, this gradient is maintained by Nodal antagonist secreted from the anterior visceral endoderm or by BMP-4 and Wnt-3 feedback loop in the extraembryonic tissues (Fig.11) <ref name="PMID25813860><pubmed>25813860</pubmed></ref>
	Nodal/Activin’s important role in heart formation is demonstrated by animal models. Presence of Activin in amphibian embryo lead to activation of heart formation whereas the absence of Nodal co-receptor ,called Cripto, in mouse embryo resulted in failure of ES cells differentiation into cardiomyocytes <ref><pubmed>20830688</pubmed></ref>. Also, knocking out copies of SMAD-2 alone or both SMAD-2 ND -3 result in inappropriate specification of axial mesoderm <ref><pubmed>12842913</pubmed></ref>.		Nodal/Activin’s important role in heart formation is demonstrated by animal models. Presence of Activin in amphibian embryo lead to activation of heart formation whereas the absence of Nodal co-receptor ,called Cripto, in mouse embryo resulted in failure of ES cells differentiation into cardiomyocytes <ref><pubmed>20830688</pubmed></ref>. Also, knocking out copies of SMAD-2 alone or both SMAD-2 ND -3 result in inappropriate specification of axial mesoderm <ref><pubmed>12842913</pubmed></ref>.

Z5018962: /* Glossary of Terms */

2017-10-26T04:39:38Z

Glossary of Terms

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	\| Group of progenitor cells that forms near the venous pole of the heart gives rise to the epicardium		\| Group of progenitor cells that forms near the venous pole of the heart gives rise to the epicardium
	\|-		\|-
			\|''' Septum transversium '''
			\| Forms from an aggregation of mesenchyme tissue that develops within the caudal part of ventral mesentery of the foregut. It is developed at day 22 in humans.
			\|--bgcolor="FAF5FF"
	\|''' Sinus venosus'''		\|''' Sinus venosus'''
	\| An early developmental cardiovascular structure, thin walled cavity, forming the input to developing heart which has 3 venous inputs (vitelline vein, umbilical vein, common cardinal vein). Later in heart development this structure gets incorporated into the wall of the future right atrium.		\| An early developmental cardiovascular structure, thin walled cavity, forming the input to developing heart which has 3 venous inputs (vitelline vein, umbilical vein, common cardinal vein). Later in heart development this structure gets incorporated into the wall of the future right atrium.
			\|-
			\|''' Subepicardium'''
			\| Situated or occurring beneath the epicardium or between the epicardium and myocardium.
	\|--bgcolor="FAF5FF"		\|--bgcolor="FAF5FF"
	\|'''Truncus arteriosus'''		\|'''Truncus arteriosus'''

Z5076019: /* Dietary supplementation of NAD in prevention of miscarriages and birth defects */

2017-10-26T04:34:41Z

Dietary supplementation of NAD in prevention of miscarriages and birth defects

← Older revision		Revision as of 14:34, 26 October 2017
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	===Dietary supplementation of NAD in prevention of miscarriages and birth defects===		===Dietary supplementation of NAD in prevention of miscarriages and birth defects===
	Sydney’s Victor Chang Cardiac Research Institute is the centre point of research to prevent recurrent miscarriages and multiple types of birth defects of the heart, ~~spinel~~, kidney and cleft palate in newborn babies.		Sydney’s Victor Chang Cardiac Research Institute is the centre point of research to prevent recurrent miscarriages and multiple types of birth defects of the heart, spine, kidney and cleft palate in newborn babies.

	Scientists have demonstrated a potential cure, in the form of a common dietary supplement. The research study found that a deficiency in a vital molecule, known as NAD, can prevent a baby’s organs from developing correctly in the womb.		Scientists have demonstrated a potential cure, in the form of a common dietary supplement. The research study found that a deficiency in a vital molecule, known as NAD, can prevent a baby’s organs from developing correctly in the womb.
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	The next step would be to develop a diagnostic test to measure NAD levels. This would enable doctors to identify the women who are at greater risk of having a baby with a birth defect, and ensure they are getting sufficient amount of vitamin B3.		The next step would be to develop a diagnostic test to measure NAD levels. This would enable doctors to identify the women who are at greater risk of having a baby with a birth defect, and ensure they are getting sufficient amount of vitamin B3.


	==Animal Models ==		==Animal Models ==

Z5018962: /* Chick Model */

2017-10-26T04:31:11Z

Chick Model

← Older revision		Revision as of 14:31, 26 October 2017
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	===Chick Model===		===Chick Model===
	Initial stages of cardiac looping involve the formation of a c-shaped tube that is curved towards the right side of the embryo. This c-shaped tube is formed as a result of ventral bending and rightward rotation. The genetic and molecular pathways involved in this process of cardiac looping have been well understand but the role mechanical forces play in this process remains poorly understood. This study on chick embryos <ref><pubmed>15282152</pubmed></ref> ~~show~~ that bending and rotation are mediated by different sets of forces. While bending is controlled by intrinsic forces to the heart, rotation into a c-shaped tube is driven by external forces exerted mainly by a membrane pushing against the heart tube called splanchnopleure (SPL). Also, some of these forces come from omphalomesenteric veins (OVs) which plays a role in the directionality of left-right looping. These results were obtained from analysis of tissue stress and strain using dissection and fluorescent labelling respectively after subjecting the embryos to mechanical perturbations.		Initial stages of cardiac looping involve the formation of a c-shaped tube that is curved towards the right side of the embryo. This c-shaped tube is formed as a result of ventral bending and rightward rotation. The genetic and molecular pathways involved in this process of cardiac looping have been well understand but the role mechanical forces play in this process remains poorly understood. This study on chick embryos <ref><pubmed>15282152</pubmed></ref> shows that bending and rotation are mediated by different sets of forces. While bending is controlled by intrinsic forces to the heart, rotation into a c-shaped tube is driven by external forces exerted mainly by a membrane pushing against the heart tube called splanchnopleure (SPL). Also, some of these forces come from omphalomesenteric veins (OVs) which plays a role in the directionality of left-right looping. These results were obtained from analysis of tissue stress and strain using dissection and fluorescent labelling respectively after subjecting the embryos to mechanical perturbations.

	Other research into chick models reveals that cardiac progenitors of the splanchnic mesoderm, cardiac neural crest and the proepicardium are the major embryonic contributors to the development of the chick heart. The contribution of these components to cardiac development occurs with precise timing and regulation during such processes as primary heart tube fusion, cardiac looping and accretion, cardiac septation and the development of the coronary vasculature. In addition to these findings, chick models revealed that one role of the anterior endoderm is to create a “cardiac field” in the overlying anterior mesoderm, and that other events will restrict this cardiac field to the region of the embryo that will become the heart later in development.<ref><pubmed> 15986452</pubmed></ref>		Other research into chick models reveals that cardiac progenitors of the splanchnic mesoderm, cardiac neural crest and the proepicardium are the major embryonic contributors to the development of the chick heart. The contribution of these components to cardiac development occurs with precise timing and regulation during such processes as primary heart tube fusion, cardiac looping and accretion, cardiac septation and the development of the coronary vasculature. In addition to these findings, chick models revealed that one role of the anterior endoderm is to create a “cardiac field” in the overlying anterior mesoderm, and that other events will restrict this cardiac field to the region of the embryo that will become the heart later in development <ref><pubmed> 15986452</pubmed></ref>.

	===Xenopus Model===		===Xenopus Model===