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Week 1 > ECM > Flashcards

ECM Flashcards

1
Q

Where is the basal lamina matrix?

A

Underlying the epithelial cells e.g. in skin, underneath villi, next to endothelial vascular cells, around Lymphatics (but only in the collecting tubules)

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2
Q

Is BL thicker or thinnger than cell? Function?

A

Much thinner, very sheet-like and provides structural support and structure for epitheilium.

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3
Q

What cells might penetrate it?

A

Patrolling yD T cells and Tmems and other Tissue resident cells (DCs need to cross and go into blood- Langerhans cross it to get to dermis).
Also leukocytes that exit blood.

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4
Q

3 main molecules that make up BL?

A

laminins, collagen IV and perlecan (a heparan sulfate proteoglycan (HSPG).

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5
Q

What strucutres does Collagen IV form in BL? What helps this?

A

Collagen has 3 a helices that wrap around each other. However these fibrils do not form fibres.
Instead the N and C terminal domain are not cleaved, allows them to interact with other collagen to form a network.
(also supercoil around other collagen fibrils a bit.)

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6
Q

What strucutre of laminins?

A

cruciform with an a B y chain.

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7
Q

What do globular heads of laminins bind with?

A

Bind with collagen.

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8
Q

What protein helps laminins bind with collagen and perlecan?

A

Nidognen.

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9
Q

What does the C terminal domain of laminins bind?

A

Binds integrins on the epithelial cells. Also binds dystoglycan (DG).

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10
Q

What does DG interact with?

A

Interacts with dystrophin (a utrohpin), if you have mutation you get muscle dystrophy.

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11
Q

What 3 states do Integrins have? What influences them?

A

Integrins have low, intermedate and high affinity binding states.
Activated by chemokines.

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12
Q

What ligands bnid to interins from BL and interstitial matrix?

A

laminins, collagen and fibronectin.

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13
Q

How do integrins increse affinity ad avidity?

A

Conformational changes upon binding and clustering.

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14
Q

How does Interstital matrix compare to BL?

A

less uniform and more diffuse, and underlies BL in soft tissue.

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15
Q

What kind of forces can interstitial matrix exert with fribonectin? How?

A

Can exert tension.
Binding of Fn to integrin on cell surface reveals Fn binding sites that cause it to interact with itself and form bundles that can exert tension.

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16
Q

What molecule can act as a sink for chemokines and cytokines and growth factors in IL matrix?

A

fibronectin.

Also have HSPGs and collagen IV).

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17
Q

What 3 moelcuels in IL matrix?

A

collagen I and III which forms a fibrillar meshwork.
hyalauronan
fibronectin

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18
Q

What small LRR molecules bind collagen 1 fibrils in IL matrix?

A

decorin./biglycan.

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19
Q

Do fibroectin bind to HPGS?

A

Yes.

20
Q

How is fibronectin improtant in wound healing?

A

Forms a provisional matrix with firbin.

21
Q

What molecules are important for wideing gaps in the BL matrix for extravasation?

A

MMPs, ADAMs, and serine proteases like elastae, plasmin.

22
Q

Which degrading products have accessory roels in remodelling BL for transit?

A

MMPs and ADAMs.

serine protease degraadation of collagen IV more important.

23
Q

What else aprat form ECM components can MMPs degrade?

A

chemokines and ctyokines.

24
Q

Degradation fragments of what in the BM provides DAMP signals?

A

Partial degradation of B1 laminins are DAMPs.

25
Q

What kind of migration is seen in IL matrix?

A

Ameboid migratino in repsonse to chemokines that is requires actin cytoskeletal rearrangement that is independent of integrins and ahdesions.

26
Q

how is TGF-B synsthesised?

A

As a homodierm with a N terminal LAP dimer that associated with disulphide bonds to LTBP.

27
Q

What clevaes LAP dimer?

A

Furin cleaves this, but TGF-B stays non-covalently bound.

LTBP-LAp and non covenletnly bound TGF bind to fibronectin.

28
Q

What two things can liberate TGF-B and what growth factor helps it tobind TGF-B receptors?

A

plasmin releases TGF B. Or intregrins on myofibroblasts bind to LAP and pull it off TGF-B.
CTGF guids TGFB to receptor.

29
Q

What siganllign does TGF-B do and what can it induce?

A

SMAD signalling and upregulates ECM and myofibroblast differentiaton.

30
Q

What receptors are at uropod and lamellipodium of migratory leukoctye?

A

uropod is CD44 and matrix bindign proteins.

At lamellipodia you have chemokine receptors.

31
Q

Chemotaxis vs haptotaxis?

A

Cehmokines simply a diffusion gradietn (by would fluid flow effect this?
Haptotaxis, chemokines sequestered by e.g. ECM molecules to resist dilution by fluid flow.

32
Q

How do HS bind to core HSPG protein?

A

heparin sulfate are made up of reapeat units that are suphated in different ways depending e.g. on tissue location (and inflammation).

HS bind via C2 basic domains.

33
Q

Do different chemokines bind different suphate patterns? What does this mean?

A

Yes, this means chemokine binding can be tissue and (inflammatory) context specific.

34
Q

In what state do chemokines bind Hs chains?

A

As dimers and oligomeres.

35
Q

Why can’t chemokines bind and bridge cell to HS? What happens instead?

A

Becuase HS and chemokine receptor bindnig sites overlap on chemokine.
Instead chemokines dissociate locally.

36
Q

How does fibronextin and collagen dense meshwork change in inflammation?

A

Dense meshwork become less dense paraell network that aids leukoctye migration, and makes amyeboid migration without support inefficient.

37
Q

what do T cells express that helps them migrate through paraell firbonectin/ collagen network?

A

activated T cells upregaulte integrins for fribronectin and collagen.

38
Q

What can HA bind?

A

Bind water and make a porous matrix, and can bind CD44 of uropod to aid leukoctye migration. Versican stailises it.

39
Q

In inflammation what can macrophages do to HA?

A

Internatise HA and produce low MW fragments.

40
Q

What can HA LW and HMW functions be?

A

LMW induces inflammatory TLR4 signalling.

HMW binds to TLR4-but can cluster TLR4 to act anit inflammatory?

41
Q

When do supramolecular complexes of HA form?

A

IN response to inflammation, and IaI (trypsin inhibitor) leaks from blood.

42
Q

How do supramolecular HA form?

A

Ia1 transferred to HA in tisseu and complexed with versican.

43
Q

What can supramolecular HA complexes do?

A

BInd CD44 with high avidity to promtoe recruitment of leukoctyes.

44
Q

what causes diff of myofibrobalsts?

A

Recruitments of macrophages produceing CTGF and TGF-B.

45
Q

What can myyfibroblasts do to cause fibrosis

A

Over secrete ECM and decrease MMP and ECM destruction.

Week 1 (7 decks)

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