Genetic lineage tracing defines myofibroblast origin and function in the injured heart methods
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Periostin expression is restricted to myofibroblasts
Next, the identity of the interstitial cell population labelled in Postn MCM/+; R26-eGFP mice was interrogated after MI injury and 2 weeks of tamoxifen treatment ( ). Hearts were harvested and serial cryosections were processed to show fibrosis and coincident eGFP + cell labelling (periostin lineage-traced) along with antibodies against vimentin, PDGFRα, αSMA, CD31, CD45 and FSP1 to identify fibroblasts or other interstitial cell types ( ). Approximately 98% of the periostin lineage-traced cells were vimentin positive, while more than half were PDGFRα-positive and ∼80% were αSMA-positive but almost none were CD31, CD45 or FSP1 reactive ( ). Consistent with these results, florescent-activated cell sorting (FACS) analysis of enzymatically isolated eGFP + cells from injured Postn MCM/+; R26-eGFP mouse hearts quantitatively confirmed the histological results, w...
Periostin expression is restricted to myofibroblasts
A recent study suggested that the type of cardiac injury might induce different populations of cells to become myofibroblasts. Hence, in addition to MI injury we also performed cardiac pressure overload by transverse aortic constriction (TAC) and infusion of the profibrotic neuroendocrine agonists, angiotensin II and phenylephrine (Ang/PE), as additional models of cardiac fibrosis. Both disease stimulations were conducted for 2 weeks in Postn MCM/+; R26-eGFP mice, concurrent with tamoxifen treatment ( and ). Both stimuli generated a large induction of periostin lineage-traced eGFP + cells throughout the heart ( ), which by immunohistochemistry were again defined as myofibroblasts ( ). One unique aspect of the pressure overload response is that eGFP + cells were concentrated within the left ventricular free wall, septum and left atria, regions of the heart that are particularly stret...
Periostin-labelled fibroblasts are functional in disease
To assess the relevance of periostin-labelled myofibroblasts during cardiac injury and fibrosis, we generated compound heterozygote mice carrying the Postn MCM allele and the Rosa26 -DTA (diphtheria toxin A) allele, which generates an inducible Cre-dependent means of killing cells in vivo ( ). Here Postn MCM/+; R26-DTA mice were given tamoxifen continuously after MI surgery and hearts from surviving mice were harvested 2 weeks afterwards ( ). Ablation of periostin + cells was verified by western blot, which showed a dramatic reduction in periostin protein in hearts of Postn MCM/+; R26-DTA mice after tamoxifen, compared with Postn MCM control mice not containing the R26-DTA allele ( ). Postn -/- heart-protein extract was used as a control. Most importantly, Postn MCM/+; R26-DTA mice subjected to MI injury showed much greater lethality in the first few days due to ventric...
Periostin lineage-tracing labels all myofibroblasts
To more definitively examine the extent to which the periostin + cells account for all of the collagen-producing myofibroblasts in the heart we also crossed the lineage-tracing Postn MCM/+; R26-tdTomato mouse with transgenic mice expressing GFP under the control of the collagen1a1 chimeric promoter ( ). The collagen1a1 promoter used to make the GFP transgene is a composite of a proximal promoter and an upstream DNase I hypersensitivity (HS4,5) region that conveys unique properties to the transgene, such that GFP is only expressed in tissue-resident fibroblasts and myofibroblasts but no other cell types ( ). The data show that nearly all periostin lineage-traced cells analysed 7 days post-MI in the injury region of the heart were collagen1a1-GFP expressing ( and ). To further determine if periostin lineage-traced cells from Postn MCM/+; R26-eGFP mice accounted for all myofibroblasts...
Origins of periostin-labelled adult cardiac fibroblasts
Myofibroblasts in the injured or diseased heart have been suggested to originate and transdifferentiate from many cellular sources, such as an endothelial cells, immune cells, smooth muscle cells, pericytes or epicardial derived resident fibroblasts. However, there is disagreement even amongst these studies each claiming that one of these cell sources is dominant. Here we attempted to quantify the cellular sources for periostin-traced myofibroblasts in the mouse heart using lineage tracing with four independent genetic loci together with concurrent periostin expression ( ). We used Rosa26 nLacZ reporter mice carrying either Tcf21 MCM (resident fibroblasts), LysM Cre (macrophages), Cdh5 Cre (endothelial cells) and Myh11 CreERT2 (smooth muscle cells) along with a periostin promoter transgene-driving ZsGreen ( ). For the lineage-tracing component, mice with inducible Cre alleles were...
Origins of periostin-labelled adult cardiac fibroblasts
As yet another criteria for determining the extent to which select cellular origins contribute to myofibroblasts in the heart, the lineage-tracing analyses with these same Cre lines was compared against a full analysis of antibody markers as presented earlier ( ). Mice were given tamoxifen food for 2 weeks, allowed 3 days off, then infarcted at 10 weeks of age and harvested 1 week later ( ). LysM Cre labelled cells primarily gave rise to CD45 and FSP1 expressing cells, but they lacked markers of fibroblasts ( and ). The Myh11 CreERT2 traced cells lacked vimentin and histological analysis showed a localization pattern to the media of vessels in the heart where smooth muscle cells reside, but not within the infarct region that would be characteristic of myofibroblasts ( and ). Endothelial cells labelled with the Cdh5 Cre allele were mostly CD31 positive and only a small portion were co-...
Origins of periostin-labelled adult cardiac fibroblasts
Since resident Tcf21 lineage-traced cells were the overwhelming source of periostin-expressing myofibroblasts in the infarct region of the heart, a more elaborate investigation of Tcf21 expression and lineage-traced cells was undertaken using Tcf21 MCM/+; R26-eGFP mice ( ). Here, we first began with uninjured mice since Tcf21 is highly expressed in tissue-resident fibroblasts at baseline within the heart. Tcf21 MCM/+; R26-eGFP mice were given tamoxifen for 2 weeks and then harvested ( ). The lineage-tracing strategy labelled large numbers of resident fibroblasts throughout the uninjured adult heart, which were positive for vimentin and PDGFRα, but not αSMA, CD31 or FSP1 ( ). These results were confirmed by quantitative FACS analysis, which again showed that all resting Tcf21 lineage-traced fibroblasts from the heart expressed vimentin but not CD31, CD45 or FSP1 ( ).
Origins of periostin-labelled adult cardiac fibroblasts
Next we performed lineage tracing after MI injury in Tcf21 MCM/+; R26-eGFP mice. Tamoxifen was given for 2 weeks before MI (with 3 days no treatment before injury), followed by harvesting of hearts 2 weeks later for analysis ( ). The results showed a 10-fold increase in total Tcf21-labelled fibroblasts in the infarct region and associated border zone, reminiscent of how periostin-labelled myofibroblasts similarly expand ( ). Immunohistochemistry-based quantification of all Tcf21 lineage-traced (eGFP + ) fibroblasts also showed a profile consistent with periostin-labelled myofibroblasts within the infarct, in that they were positive for vimentin, αSMA and PDGFRα ( ). To further characterize Tcf21-expressing cells in a similar mouse model of ischaemia-reperfusion (I/R) injury to the heart, a Tcf21 LacZ knock-in allele was used to mark currently expressing fibroblasts ( ). An...
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Next, the identity of the interstitial cell population labelled in Postn MCM/+; R26-eGFP mice was interrogated after MI injury and 2 weeks of tamoxifen treatment ( ). Hearts were harvested and serial cryosections were processed to show fibrosis and coincident eGFP + cell labelling (periostin lineage-traced) along with antibodies against vimentin, PDGFRα, αSMA, CD31, CD45 and FSP1 to identify fibroblasts or other interstitial cell types ( ). Approximately 98% of the periostin lineage-traced cells were vimentin positive, while more than half were PDGFRα-positive and ∼80% were αSMA-positive but almost none were CD31, CD45 or FSP1 reactive ( ). Consistent with these results, florescent-activated cell sorting (FACS) analysis of enzymatically isolated eGFP + cells from injured Postn MCM/+; R26-eGFP mouse hearts quantitatively confirmed the histological results, with nearly an identical marker profile ( ). Thy1 was also uniquely used in the FACS analysis since it is a surface marker and it has been reported to identify fibroblasts ( ). Since the presence of vimentin reactivity and absence of CD31 and CD45 reactivity is a criterion for total fibroblast identi...
A recent study suggested that the type of cardiac injury might induce different populations of cells to become myofibroblasts. Hence, in addition to MI injury we also performed cardiac pressure overload by transverse aortic constriction (TAC) and infusion of the profibrotic neuroendocrine agonists, angiotensin II and phenylephrine (Ang/PE), as additional models of cardiac fibrosis. Both disease stimulations were conducted for 2 weeks in Postn MCM/+; R26-eGFP mice, concurrent with tamoxifen treatment ( and ). Both stimuli generated a large induction of periostin lineage-traced eGFP + cells throughout the heart ( ), which by immunohistochemistry were again defined as myofibroblasts ( ). One unique aspect of the pressure overload response is that eGFP + cells were concentrated within the left ventricular free wall, septum and left atria, regions of the heart that are particularly stretched in response to pressure overload, but less so in the right ventricle and right atria ( ). In contrast, eGFP + cellular distribution was more uniform throughout the entire heart with 2 weeks of Ang/PE stimulation ( ). Taken together, these data suggest that periostin lineage-tracing identifies m...
To assess the relevance of periostin-labelled myofibroblasts during cardiac injury and fibrosis, we generated compound heterozygote mice carrying the Postn MCM allele and the Rosa26 -DTA (diphtheria toxin A) allele, which generates an inducible Cre-dependent means of killing cells in vivo ( ). Here Postn MCM/+; R26-DTA mice were given tamoxifen continuously after MI surgery and hearts from surviving mice were harvested 2 weeks afterwards ( ). Ablation of periostin + cells was verified by western blot, which showed a dramatic reduction in periostin protein in hearts of Postn MCM/+; R26-DTA mice after tamoxifen, compared with Postn MCM control mice not containing the R26-DTA allele ( ). Postn -/- heart-protein extract was used as a control. Most importantly, Postn MCM/+; R26-DTA mice subjected to MI injury showed much greater lethality in the first few days due to ventricular wall rupture, which is consistent with lethality in Postn -/- mice subject to the same injury due to a defect in the formation of a protective scar, or in a subset of developing embryos when collagen-dependent structural regions are formed in the cardiovascular system in and around...
To more definitively examine the extent to which the periostin + cells account for all of the collagen-producing myofibroblasts in the heart we also crossed the lineage-tracing Postn MCM/+; R26-tdTomato mouse with transgenic mice expressing GFP under the control of the collagen1a1 chimeric promoter ( ). The collagen1a1 promoter used to make the GFP transgene is a composite of a proximal promoter and an upstream DNase I hypersensitivity (HS4,5) region that conveys unique properties to the transgene, such that GFP is only expressed in tissue-resident fibroblasts and myofibroblasts but no other cell types ( ). The data show that nearly all periostin lineage-traced cells analysed 7 days post-MI in the injury region of the heart were collagen1a1-GFP expressing ( and ). To further determine if periostin lineage-traced cells from Postn MCM/+; R26-eGFP mice accounted for all myofibroblasts in the heart we performed single-cell sorting by Fluidigm followed by RNAseq analysis after MI injury, versus uninjured hearts. Analysis of the transcriptome from 185 individual cells that passed quality assurance (see Methods) was performed from the hearts of MI injured and sham mice, and 63 of the...
Myofibroblasts in the injured or diseased heart have been suggested to originate and transdifferentiate from many cellular sources, such as an endothelial cells, immune cells, smooth muscle cells, pericytes or epicardial derived resident fibroblasts. However, there is disagreement even amongst these studies each claiming that one of these cell sources is dominant. Here we attempted to quantify the cellular sources for periostin-traced myofibroblasts in the mouse heart using lineage tracing with four independent genetic loci together with concurrent periostin expression ( ). We used Rosa26 nLacZ reporter mice carrying either Tcf21 MCM (resident fibroblasts), LysM Cre (macrophages), Cdh5 Cre (endothelial cells) and Myh11 CreERT2 (smooth muscle cells) along with a periostin promoter transgene-driving ZsGreen ( ). For the lineage-tracing component, mice with inducible Cre alleles were given tamoxifen for 2 weeks, then given MI injury 3 days later, while the two other mouse lines had constitutive and non-regulated Cre alleles and thus had continuous labelling ( ). Hearts were processed for antibody detection of nuclear localized LacZ (β-galactosidase) versus ZsGreen expressio...
As yet another criteria for determining the extent to which select cellular origins contribute to myofibroblasts in the heart, the lineage-tracing analyses with these same Cre lines was compared against a full analysis of antibody markers as presented earlier ( ). Mice were given tamoxifen food for 2 weeks, allowed 3 days off, then infarcted at 10 weeks of age and harvested 1 week later ( ). LysM Cre labelled cells primarily gave rise to CD45 and FSP1 expressing cells, but they lacked markers of fibroblasts ( and ). The Myh11 CreERT2 traced cells lacked vimentin and histological analysis showed a localization pattern to the media of vessels in the heart where smooth muscle cells reside, but not within the infarct region that would be characteristic of myofibroblasts ( and ). Endothelial cells labelled with the Cdh5 Cre allele were mostly CD31 positive and only a small portion were co-labelled for vimentin, while none were αSMA expressing further suggesting that endogenous endothelial cell lineages do not generate myofibroblasts in the heart with MI injury ( and ). Thus, endothelial cells, smooth muscle cells and immune cells are negligible sources for generating myofibrobla...
Since resident Tcf21 lineage-traced cells were the overwhelming source of periostin-expressing myofibroblasts in the infarct region of the heart, a more elaborate investigation of Tcf21 expression and lineage-traced cells was undertaken using Tcf21 MCM/+; R26-eGFP mice ( ). Here, we first began with uninjured mice since Tcf21 is highly expressed in tissue-resident fibroblasts at baseline within the heart. Tcf21 MCM/+; R26-eGFP mice were given tamoxifen for 2 weeks and then harvested ( ). The lineage-tracing strategy labelled large numbers of resident fibroblasts throughout the uninjured adult heart, which were positive for vimentin and PDGFRα, but not αSMA, CD31 or FSP1 ( ). These results were confirmed by quantitative FACS analysis, which again showed that all resting Tcf21 lineage-traced fibroblasts from the heart expressed vimentin but not CD31, CD45 or FSP1 ( ).
Next we performed lineage tracing after MI injury in Tcf21 MCM/+; R26-eGFP mice. Tamoxifen was given for 2 weeks before MI (with 3 days no treatment before injury), followed by harvesting of hearts 2 weeks later for analysis ( ). The results showed a 10-fold increase in total Tcf21-labelled fibroblasts in the infarct region and associated border zone, reminiscent of how periostin-labelled myofibroblasts similarly expand ( ). Immunohistochemistry-based quantification of all Tcf21 lineage-traced (eGFP + ) fibroblasts also showed a profile consistent with periostin-labelled myofibroblasts within the infarct, in that they were positive for vimentin, αSMA and PDGFRα ( ). To further characterize Tcf21-expressing cells in a similar mouse model of ischaemia-reperfusion (I/R) injury to the heart, a Tcf21 LacZ knock-in allele was used to mark currently expressing fibroblasts ( ). An I/R model often generates a smaller injury area compared with MI so that expansion can be better examined. While the uninjured heart again showed expression in tissue-resident fibroblasts throughout the heart (corresponding to ∼10% of the total cell number in the heart), areas of direct injury...
Machine-readable layer
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"text": "Next we performed lineage tracing after MI injury in Tcf21 MCM/+; R26-eGFP mice. Tamoxifen was given for 2 weeks before MI (with 3 days no treatment before injury), followed by harvesting of hearts 2 weeks later for analysis ( ). The results showed a 10-fold increase in total Tcf21-labelled fibroblasts in the infarct region and associated border zone, reminiscent of how periostin-labelled myofibroblasts similarly expand ( ). Immunohistochemistry-based quantification of all Tcf21 lineage-traced (eGFP + ) fibroblasts also showed a profile consistent with periostin-labelled myofibroblasts within the infarct, in that they were positive for vimentin, αSMA and PDGFRα ( ). To further characterize Tcf21-expressing cells in a similar mouse model of ischaemia-reperfusion (I/R) injury to the heart, a Tcf21 LacZ knock-in allele was used to mark currently expressing fibroblasts ( ). An..."
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