Abnormal Development - Maternal Inflammation - Revision history

Z8600021 at 12:12, 19 March 2018

2018-03-19T12:12:20Z

← Older revision		Revision as of 23:12, 19 March 2018
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	* '''Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse.'''~~<ref><pubmed>~~21935422~~</pubmed></ref>~~ "Cellular uptake of proteins from the cerebrospinal fluid was observed in brains from lipopolysaccharide-treated animals in radial progenitor cells. However, the foetal blood-brain barrier to plasma proteins remained intact. Together, these results indicate that maternal inflammation can disrupt the ventricular surface and lead to decreased cellular proliferation. Changes in cell density in Layers IV and V at post-natal Day 8 show that these initial changes have prolonged effects on cortical organization. The possible shift in the fate of progeny and the resulting alterations in the relative cell numbers in the cerebral cortex following a maternal inflammatory response shown here will require further investigation to determine the long-term consequences of inflammation on the development of neuronal circuitry and behaviour."		* '''Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse.'''{{#pmid:21935422\|PMID21935422}} "Cellular uptake of proteins from the cerebrospinal fluid was observed in brains from lipopolysaccharide-treated animals in radial progenitor cells. However, the foetal blood-brain barrier to plasma proteins remained intact. Together, these results indicate that maternal inflammation can disrupt the ventricular surface and lead to decreased cellular proliferation. Changes in cell density in Layers IV and V at post-natal Day 8 show that these initial changes have prolonged effects on cortical organization. The possible shift in the fate of progeny and the resulting alterations in the relative cell numbers in the cerebral cortex following a maternal inflammatory response shown here will require further investigation to determine the long-term consequences of inflammation on the development of neuronal circuitry and behaviour."
	* '''Systemic maternal inflammation and neonatal hyperoxia induces remodeling and left ventricular dysfunction in mice'''~~<ref><pubmed>~~21964917~~</pubmed></ref>~~ "These results demonstrate that systemic maternal inflammation combined with neonatal hyperoxia exposure induces alterations in cardiac structure and function leading to cardiac failure in adulthood and supports the importance of the intrauterine and neonatal milieu on adult health."
			* '''Systemic maternal inflammation and neonatal hyperoxia induces remodeling and left ventricular dysfunction in mice'''{{#pmid:21964917\|PMID21964917}} "These results demonstrate that systemic maternal inflammation combined with neonatal hyperoxia exposure induces alterations in cardiac structure and function leading to cardiac failure in adulthood and supports the importance of the intrauterine and neonatal milieu on adult health."
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	{\| class="wikitable mw-collapsible mw-collapsed"		{\| class="wikitable mw-collapsible mw-collapsed"
	! More recent papers		! More recent papers
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	\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}		\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}
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	===Reviews===		===Reviews===
	~~<pubmed></pubmed>~~
	===Articles===		===Articles===
	~~<pubmed>~~21376162~~</pubmed>~~		{{#pmid:21376162}}
	~~<pubmed>21771319</pubmed>~~
	~~<pubmed>16489598</pubmed>~~

			{{#pmid:21771319}}

			{{#pmid:16489598}}

	===Search Pubmed===		===Search Pubmed===

Z8600021 at 04:44, 3 December 2014

2014-12-03T04:44:26Z

← Older revision		Revision as of 15:44, 3 December 2014
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			{{Header}}

	{{Educational Warning}}		{{Educational Warning}}

	==Introduction==		==Introduction==


	:{{~~Template:~~Environmental}}		{{Environmental}}

	:{{Viral Links}}		{{Viral Links}}

	==Some Recent Findings==		==Some Recent Findings==
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	* '''Systemic maternal inflammation and neonatal hyperoxia induces remodeling and left ventricular dysfunction in mice'''<ref><pubmed>21964917</pubmed></ref> "These results demonstrate that systemic maternal inflammation combined with neonatal hyperoxia exposure induces alterations in cardiac structure and function leading to cardiac failure in adulthood and supports the importance of the intrauterine and neonatal milieu on adult health."		* '''Systemic maternal inflammation and neonatal hyperoxia induces remodeling and left ventricular dysfunction in mice'''<ref><pubmed>21964917</pubmed></ref> "These results demonstrate that systemic maternal inflammation combined with neonatal hyperoxia exposure induces alterations in cardiac structure and function leading to cardiac failure in adulthood and supports the importance of the intrauterine and neonatal milieu on adult health."
	\|}		\|}
			{\| class="wikitable mw-collapsible mw-collapsed"
			! More recent papers
			\|-
			\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}

			Search term: [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=search&term=Maternal%20Inflammation ''Maternal Inflammation'']

			<pubmed limit=5>Maternal Inflammation</pubmed>
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	==References==		==References==

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	== External Links ==		== External Links ==
			{{External Links}}

			{{Glossary}}


	{{~~Template:Glossary}}~~		{{Footer}}
	~~{{Template:~~Footer}}


	[[Category:Abnormal Development]] [[Category:Environmental Abnormalities]]		[[Category:Abnormal Development]] [[Category:Environmental Abnormalities]]

S8600021: /* Some Recent Findings */

2012-02-16T22:12:18Z

Some Recent Findings

← Older revision		Revision as of 09:12, 17 February 2012
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	* '''Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse.'''<ref><pubmed>~~21964917~~</pubmed></ref> "Cellular uptake of proteins from the cerebrospinal fluid was observed in brains from lipopolysaccharide-treated animals in radial progenitor cells. However, the foetal blood-brain barrier to plasma proteins remained intact. Together, these results indicate that maternal inflammation can disrupt the ventricular surface and lead to decreased cellular proliferation. Changes in cell density in Layers IV and V at post-natal Day 8 show that these initial changes have prolonged effects on cortical organization. The possible shift in the fate of progeny and the resulting alterations in the relative cell numbers in the cerebral cortex following a maternal inflammatory response shown here will require further investigation to determine the long-term consequences of inflammation on the development of neuronal circuitry and behaviour."		* '''Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse.'''<ref><pubmed>21935422</pubmed></ref> "Cellular uptake of proteins from the cerebrospinal fluid was observed in brains from lipopolysaccharide-treated animals in radial progenitor cells. However, the foetal blood-brain barrier to plasma proteins remained intact. Together, these results indicate that maternal inflammation can disrupt the ventricular surface and lead to decreased cellular proliferation. Changes in cell density in Layers IV and V at post-natal Day 8 show that these initial changes have prolonged effects on cortical organization. The possible shift in the fate of progeny and the resulting alterations in the relative cell numbers in the cerebral cortex following a maternal inflammatory response shown here will require further investigation to determine the long-term consequences of inflammation on the development of neuronal circuitry and behaviour."
			* '''Systemic maternal inflammation and neonatal hyperoxia induces remodeling and left ventricular dysfunction in mice'''<ref><pubmed>21964917</pubmed></ref> "These results demonstrate that systemic maternal inflammation combined with neonatal hyperoxia exposure induces alterations in cardiac structure and function leading to cardiac failure in adulthood and supports the importance of the intrauterine and neonatal milieu on adult health."
	\|}		\|}


	==References==		==References==

S8600021: /* References */

2012-02-16T22:09:04Z

References

← Older revision		Revision as of 09:09, 17 February 2012
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	===Reviews===		===Reviews===
			<pubmed></pubmed>
			===Articles===
			<pubmed>21376162</pubmed>
			<pubmed>21771319</pubmed>
			<pubmed>16489598</pubmed>

	~~===Articles===~~
	~~<pubmed></pubmed>~~


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	'''Search Pubmed:''' [http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=Maternal+Inflammation Maternal Inflammation]		'''Search Pubmed:''' [http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=Maternal+Inflammation Maternal Inflammation]

	== External Links ==		== External Links ==

S8600021 at 22:06, 16 February 2012

2012-02-16T22:06:48Z

← Older revision		Revision as of 09:06, 17 February 2012
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			{{Educational Warning}}

	==Introduction==		==Introduction==

S8600021 at 21:38, 16 February 2012

2012-02-16T21:38:40Z

← Older revision		Revision as of 08:38, 17 February 2012
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			==Introduction==


	:{{Template:Environmental}}		:{{Template:Environmental}}

	~~:{{Bacterial Links}}~~

	:{{Viral Links}}		:{{Viral Links}}

S8600021 at 21:37, 16 February 2012

2012-02-16T21:37:10Z

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-==2011==
+:{{Bacterial Links}}
-===Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse===
+:{{Viral Links}}
-Brain. 2011 Nov;134(Pt 11):3236-48. Epub 2011 Sep 29.
+==Some Recent Findings==
-Stolp HB, Turnquist C, Dziegielewska KM, Saunders NR, Anthony DC, Molnár Z.
+|}
-It has been well established that maternal inflammation during pregnancy alters neurological function in the offspring, but its impact on cortical development and long-term consequences on the cytoarchitecture is largely unstudied. Here we report that lipopolysaccharide-induced systemic maternal inflammation in C57Bl/6 mice at embryonic Day 13.5 of pregnancy, as early as 8 h after challenge, caused a significant reduction in cell proliferation in the ventricular zone of the developing cerebral cortex, as revealed by quantification of anti-phospho-Histone H3 immunoreactivity and bromodeoxyuridine pulse labelling. The angle of mitotic cleavage, determined from analysis of haematoxylin and eosin staining, cyclin E1 gene expression and the pattern of β-catenin immunoreactivity were also altered by the challenge, which suggests a change from symmetric to asymmetric division in the radial progenitor cells. Modifications of cortical lamination and gene expression patterns were detected at post-natal Day 8 suggesting prolonged consequences of these alterations during embryonic development. Cellular uptake of proteins from the cerebrospinal fluid was observed in brains from lipopolysaccharide-treated animals in radial progenitor cells. However, the foetal blood-brain barrier to plasma proteins remained intact. Together, these results indicate that maternal inflammation can disrupt the ventricular surface and lead to decreased cellular proliferation. Changes in cell density in Layers IV and V at post-natal Day 8 show that these initial changes have prolonged effects on cortical organization. The possible shift in the fate of progeny and the resulting alterations in the relative cell numbers in the cerebral cortex following a maternal inflammatory response shown here will require further investigation to determine the long-term consequences of inflammation on the development of neuronal circuitry and behaviour.
+==References==
-PMID 21964917
+<references/>

S8600021: Created page with " ==2011== ===Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse=== Brain. 2011 Nov;134(Pt 11):3236-48. Epub 2011 Sep 29. St..."

2012-02-16T21:33:50Z

Created page with " ==2011== ===Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse=== Brain. 2011 Nov;134(Pt 11):3236-48. Epub 2011 Sep 29. St..."

New page

==2011==

===Reduced ventricular proliferation in the foetal cortex following maternal inflammation in the mouse===

Brain. 2011 Nov;134(Pt 11):3236-48. Epub 2011 Sep 29.

Stolp HB, Turnquist C, Dziegielewska KM, Saunders NR, Anthony DC, Molnár Z.
Source
Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3QX, UK. helen.stolp@dpag.ox.ac.uk

Abstract

It has been well established that maternal inflammation during pregnancy alters neurological function in the offspring, but its impact on cortical development and long-term consequences on the cytoarchitecture is largely unstudied. Here we report that lipopolysaccharide-induced systemic maternal inflammation in C57Bl/6 mice at embryonic Day 13.5 of pregnancy, as early as 8 h after challenge, caused a significant reduction in cell proliferation in the ventricular zone of the developing cerebral cortex, as revealed by quantification of anti-phospho-Histone H3 immunoreactivity and bromodeoxyuridine pulse labelling. The angle of mitotic cleavage, determined from analysis of haematoxylin and eosin staining, cyclin E1 gene expression and the pattern of β-catenin immunoreactivity were also altered by the challenge, which suggests a change from symmetric to asymmetric division in the radial progenitor cells. Modifications of cortical lamination and gene expression patterns were detected at post-natal Day 8 suggesting prolonged consequences of these alterations during embryonic development. Cellular uptake of proteins from the cerebrospinal fluid was observed in brains from lipopolysaccharide-treated animals in radial progenitor cells. However, the foetal blood-brain barrier to plasma proteins remained intact. Together, these results indicate that maternal inflammation can disrupt the ventricular surface and lead to decreased cellular proliferation. Changes in cell density in Layers IV and V at post-natal Day 8 show that these initial changes have prolonged effects on cortical organization. The possible shift in the fate of progeny and the resulting alterations in the relative cell numbers in the cerebral cortex following a maternal inflammatory response shown here will require further investigation to determine the long-term consequences of inflammation on the development of neuronal circuitry and behaviour.

PMID 21964917